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Hengrui Pharma Reports Q1 2026 Results with Revenue and Net Profit Growth

On April 22, 2026 Hengrui Pharma reported steady growth in the first quarter of 2026. In Q1 2026, the Company recorded revenue of RMB 8.14 billion, up 12.98% year-over-year, while net profit attributable to shareholders increased by 21.78% to RMB 2.28 billion. Innovative drugs remained the key growth driver, generating RMB 4.53 billion in revenue, up 25.75% year-over-year and accounting for 61.69% of total pharmaceutical sales.

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The Company continued to advance its innovation-driven strategy with sustained R&D investment and solid pipeline progress. R&D investments in Q1 2026 totaled RMB 2.22 billion, representing for approximately 27.32% of revenue.

During the period, three innovative products and new indications were approved in China, which included an anti-PD-L1/TGF-βRII bi-functional fusion protein and an indication expansion for HER2-targeting ADC.

In terms of pipeline advancement, the Company obtained 26 clinical trial approvals and had 8 new drug applications accepted in China across key therapeutic areas including oncology, metabolic, cardiovascular, and immunological diseases.

Business development has become a recurring and increasingly important growth driver, with RMB 787 million in out-licensing revenue recognized during the quarter, primarily from the collaboration with GSK. Since 2023, Hengrui Pharma has completed 12 overseas business development transactions, including out-licensing, NewCo structures, and strategic alliance models.

A key milestone during the period was the successful Nasdaq listing of Kailera Therapeutics (NASDAQ: KLRA), a NewCo company built around Hengrui Pharma’s GLP-1-based assets. This milestone reflects continued progress in executing the Company’s NewCo strategy, with Hengrui and Kailera working together to advance the global development of the GLP-1 portfolio.

Looking ahead, Hengrui Pharma will remain committed to innovation and globalization, strengthening its pipeline and advancing the development and commercialization of innovative therapies to benefit patients worldwide.

(Press release, Hengrui Pharmaceuticals, APR 22, 2026, View Source [SID1234664700])

Phanes Therapeutics to Present Updated Phase 2 Clinical Trial Results of Spevatamig (PT886) in Combination with Chemotherapy in Frontline Treatment of Metastatic PDAC at the 2026 ASCO Annual Meeting

On April 22, 2026 Phanes Therapeutics, Inc. (Phanes), a clinical stage biotech company focused on innovative drug discovery and development in oncology, reported that they will present updated Phase 2 results of spevatamig (PT886) in combination with chemotherapy in frontline (1L) treatment of metastatic pancreatic ductal adenocarcinoma (mPDAC) at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting held on May 29 – June 2, 2026 in Chicago. Details of the presentation are below:

Title: Spevatamig (PT886), a claudin 18.2 (CLDN18.2)/CD47 bispecific antibody, in combination with gemcitabine plus nab-paclitaxel (GnP) in frontline (1L) treatment of metastatic pancreatic ductal adenocarcinoma (mPDAC)

Date/Time: May 30, 2026, 9:00 AM-12:00 PM CDT

Session: Gastrointestinal Cancer – Gastroesophageal, Pancreatic, and Hepatobiliary

Abstract #: 4192

Poster #: 175

First Author: Anwaar Saeed, MD, University of Pittsburgh Medical Center

ABOUT SPEVATAMIG

Spevatamig is a first-in-class native IgG-like bispecific antibody (bsAb) targeting claudin 18.2 and CD47. It was granted orphan drug designation (ODD) for the treatment of pancreatic cancer by the FDA in 2022 and was granted Fast Track designation for the treatment of patients with metastatic claudin 18.2-positive pancreatic adenocarcinoma in 2024. In 2023, Phanes entered into a clinical collaboration agreement with Merck (known as MSD outside the US and Canada) to study spevatamig in combination with pembrolizumab.

Phanes is conducting clinical trials with spevatamig in multiple cancer indications, including a Phase 2 study evaluating the efficacy of spevatamig in combination with chemotherapy in first-line PDAC patients. As of April 2026, 180 patients globally have been dosed with spevatamig collectively in monotherapy and combination therapy settings.

(Press release, Phanes Therapeutics, APR 22, 2026, View Source [SID1234664699])

Altimmune Announces Pricing of $225 Million Oversubscribed Public Offering of Securities

On April 22, 2026 Altimmune, Inc. (Nasdaq: ALT), a late clinical-stage biopharmaceutical company developing pemvidutide to address serious liver diseases, reported the pricing of its previously announced underwritten public offering consisting of (i) 64,250,000 shares of its common stock and accompanying common stock warrants to purchase an aggregate of 64,250,000 shares of common stock (or pre-funded warrants in lieu thereof) and (ii) in lieu of common stock, to certain investors that so choose, pre-funded warrants to purchase an aggregate of up to 10,750,000 shares of its common stock and accompanying common stock warrants to purchase an aggregate of 10,750,000 shares of common stock (or pre-funded warrants in lieu thereof), at an exercise price of $0.001 per pre-funded warrant. The common stock and pre-funded warrants are being sold in combination with an accompanying common stock warrant to purchase one share of common stock (or pre-funded warrant in lieu thereof) issued for each share of common stock or pre-funded warrant sold. The accompanying common stock warrant has an exercise price of $3.00 per share, is immediately exercisable from the date of issuance and will expire upon the earlier of (i) the fifth anniversary of the original issuance date and (ii) forty-five days following the Company’s public announcement of a successful data readout of its Phase 3 trial of pemvidutide in metabolic dysfunction-associated steatohepatitis ("MASH"). The combined offering price of each share of common stock and accompany common stock warrant is $3.00. The combined offering price of each pre-funded warrant and accompanying common stock warrant is $2.999. The offering is expected to close on or about April 24, 2026, subject to satisfaction of customary closing conditions.

All of the shares, pre-funded warrants and accompanying common stock warrants in the offering are being sold by Altimmune. The gross proceeds from the offering before deducting underwriting discounts and commissions and other offering expenses, are expected to be approximately $225 million. The public offering is subject to market and other conditions, and there can be no assurance as to whether or when the public offering may be completed.

Altimmune intends to use the net proceeds from this offering to fund its upcoming Phase 3 trial in MASH, as well as for working capital and general corporate purposes.

Leerink Partners and Barclays are acting as joint bookrunning managers for the offering. Titan Partners is acting as co-bookrunning manager for the offering.

The shares of common stock, pre-funded warrants, common stock warrants and shares of common stock issuable upon the exercise of the pre-funded warrants and common stock warrants are being offered by Altimmune pursuant to two effective shelf registration statements on Form S-3 that were previously filed with the U.S. Securities and Exchange Commission (SEC) and declared effective by the SEC on December 5, 2025 and March 13, 2025, respectively, and a related registration statement that was filed with the SEC on April 22, 2026 pursuant to Rule 462(b) under the Securities Act of 1933, as amended (and became automatically effective upon filing). The preliminary prospectus supplement and accompanying prospectuses relating to and describing the terms of the offering were filed with the SEC on April 22, 2026 and are available on the SEC’s website located at www.sec.gov. Electronic copies of the final prospectus supplement may be obtained, when available, by contacting Leerink Partners LLC, Syndicate Department, 53 State Street, 40th Floor, Boston, MA 02109, or by telephone at (800) 808-7525 ext. 6105, or by email at [email protected]; Barclays Capital Inc., c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717, by telephone at (888) 603-5847, or by email at [email protected]; or by accessing the SEC’s website at www.sec.gov. Before you invest, you should read the preliminary prospectus supplement and accompanying prospectuses and other documents Altimmune has filed with the SEC that are incorporated by reference into the preliminary prospectus supplement and accompanying prospectuses for more complete information about Altimmune and the offering.

This press release shall not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or 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 jurisdiction.

(Press release, Altimmune, APR 22, 2026, View Source [SID1234664698])

Actinium Highlights Transcriptional Reprogramming as a Key Mechanism Underpinning Mutation-Agnostic Activity of Actimab-A in AML at the 2026 American Association of Cancer Research Annual Meeting

On April 22, 2026 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, reported data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting supporting transcriptional reprogramming as a central mechanism driving the mutation-agnostic anti-leukemic activity of Actimab-A (lintuzumab-Ac225) in acute myeloid leukemia (AML).

Preclinical translational data demonstrated that lintuzumab-Ac225 delivers potent cytotoxic activity across AML models harboring common mutations, including FLT3, NPM1, KMT2A, and TP53, as well as in primary patient samples. Importantly, combining Actimab-A with standard-of-care therapies – the menin inhibitor revumenib, the FLT3 inhibitor gilteritinib, and the hypomethylating agent azacitidine – resulted in enhanced leukemic cell killing in vivo across all tested models, independent of mutation status. These results support a combination-driven clinical strategy aimed at improving depth and durability of response. The findings provide the mechanistic foundation for Actimab-A’s observed clinical activity and, together with the manageable safety profile demonstrated across prior Actimab-A trials in more than 150 AML patients, reinforce its suitability as a combination backbone across multiple treatment settings.

Actimab-A is Actinium’s lead clinical radiotherapy delivering Actinium-225, a potent alpha-emitter radioisotope payload that produces lethal double-strand DNA breaks to kill CD33-expressing AML cells. CD33 is expressed ubiquitously in AML and other myeloid malignancies. Actimab-A has been evaluated in more than 150 AML patients across multiple treatment settings, including as monotherapy and in combination with the chemotherapy regimen CLAG-M and with the BCL-2 inhibitor venetoclax, where it has demonstrated compelling clinical activity and a manageable safety profile. Under our Cooperative Research and Development Agreement (CRADA) with the National Cancer Institute (NCI), Actimab-A is being advanced through the NCI’s National Clinical Trials Network, including an ongoing frontline triplet trial combining Actimab-A with venetoclax and the hypomethylating agent ASTX-727 in newly diagnosed AML patients. The data presented at AACR (Free AACR Whitepaper) 2026 further support Actimab-A’s mutation-agnostic mechanism of action and its synergistic activity with targeted therapies approved for patients with the most commonly expressed AML mutations.

Key Data and Highlights of the Actimab-A AACR (Free AACR Whitepaper) Presentation

New data on Actimab-A’s mechanism and combination potential in primary AML patient samples further support its positioning as a foundational backbone therapy across multiple AML treatment settings, significantly expanding its commercial opportunity across the AML treatment continuum. In the relapsed/refractory AML setting Actimab-A in combination with the intensive chemotherapy regimen CLAG-M produced an 83% overall response rate and 75% MRD-negativity in a Phase 1 trial which forms the basis of a Phase 2/3 registrational study for which Actinium has FDA alignment and is seeking a development partner. Actimab-A is also being studied in newly diagnosed patients via the ongoing NCI-sponsored frontline triplet trial of Actimab-A with venetoclax and ASTX-727; and has shown promise in post-remission and MRD-directed settings; as well as myelodysplastic syndrome (MDS) and other CD33-expressing myeloid malignancies.

Transcriptional Reprogramming as a Key Mechanism for Actimab-A Combination Activity

Combination treatment produced consistent pathway-level changes compared with monotherapy. Gene set enrichment analyses (GSEA) showed enhanced myeloid differentiation signatures with the addition of Actimab-A (lintuzumab-Ac225) to revumenib, gilteritinib, and azacitidine.

Across models, combinations were associated with downregulation of proliferative programs, including MYC target genes, E2F targets, and G2/M checkpoint signatures, together with enrichment of p53-associated stress response and apoptosis pathways.

Together, these findings show that Actimab-A combinations don’t just add cytotoxicity — they reprogram AML cells from proliferation toward differentiation and apoptosis, providing the mechanistic basis for deeper, more durable MRD-negative responses and reinforcing Actimab-A’s role as a universal combination backbone across AML.

Broad Activity of Actimab-A as Monotherapy and in Combination in Primary AML Patient Samples

Actimab-A (LinT-Ac225) showed robust cytotoxicity in primary AML patient samples, independent of FLT3, KMT2A, NPM1, IDH1, IDH2, or TP53 mutation status, positioning Actimab-A to treat the full AML population, including TP53-mutant patients who lack effective targeted options, and to serve as a universal combination partner rather than a mutation-restricted therapy.

Combining standard-of-care therapies (SOC) – revumenib (menin-KMT2A inhibitor), gilteritinib (FLT3 inhibitor), and azacitidine (hypomethylating agent) – with Actimab-A enhanced anti-leukemic efficacy across models – demonstrating synergy with one drug from each of the three pillars of modern AML care (targeted kinase inhibitors, menin inhibitors, and hypomethylating agents) and supporting Actimab-A’s positioning as a universal combination partner across frontline, relapsed/refractory, and unfit AML populations.

Sandesh Seth, Actinium’s Chairman and CEO, said, "The data presented at AACR (Free AACR Whitepaper) 2026 represent a significant step forward in our mission to establish Actimab-A as the foundational backbone therapy across the AML treatment continuum. For the first time, we have clear molecular evidence – through transcriptional profiling – of how Actimab-A reprograms AML cells to activate p53-driven apoptosis and shut down proliferative signaling, providing the mechanistic basis for deeper, more durable MRD-negative responses and mutation-agnostic activity we have consistently observed clinically. As the only CD33-targeted radiotherapy in development for myeloid malignancies, Actimab-A uniquely leverages the broad, stable expression of CD33 and the potent, mutation-agnostic Ac-225 payload to complement – not compete with – the targeted therapies that define today’s AML standard of care. Building on compelling clinical results across more than 150 patients in multiple treatment settings, and the high visibility of our NCI CRADA – including the ongoing frontline triplet trial with venetoclax and ASTX-727 – these findings will strengthen investigator enthusiasm for Actimab-A and reinforce the significant commercial opportunity ahead as we seek a partner for the registrational Phase 2/3 Actimab-A + CLAG-M study for which we have FDA alignment. We are focused on executing across our ongoing and planned clinical programs to deliver meaningful improvements in outcomes for AML patients, who continue to face high unmet medical need that is not addressed by currently available therapies."

The Actimab-A AACR (Free AACR Whitepaper) presentation is available for viewing on the Presentations & Webinars page of Actinium’s website HERE.

Title: Actimab-A, a CD33-Targeted Actinium-225 Radioconjugate, Drives Mutation-Agnostic Anti-Leukemic Activity and Synergizes with Standard Therapies in AML Through Transcriptional Reprogramming

Abstract Number: 5827

About Actimab-A

Actimab-A (lintuzumab-Ac225) is Actinium’s lead CD33-targeted radiotherapy and the only CD33-targeted radiotherapy in clinical development for myeloid malignancies. Actimab-A pairs a humanized anti-CD33 monoclonal antibody (lintuzumab) with the potent alpha-emitter Actinium-225 (Ac-225), which delivers high-energy, short-range radiation that produces lethal double-strand DNA breaks in CD33-expressing leukemic cells while sparing surrounding healthy tissue. Because CD33 is expressed on the blasts of the large majority of AML patients and the Ac-225 payload kills cells independent of genetic background, Actimab-A is positioned as a mutation-agnostic backbone that can be combined with the targeted and non-targeted therapies that define today’s AML standard of care.

Actimab-A has been studied in more than 150 patients with AML across multiple treatment settings, including as monotherapy and in combination with the intensive chemotherapy regimen CLAG-M and with the BCL-2 inhibitor venetoclax. In a Phase 1 trial in relapsed/refractory AML, Actimab-A plus CLAG-M produced an 83% overall response rate and 75% MRD-negativity at the recommended Phase 2 dose, with meaningful overall survival benefits in a high-risk population including patients with TP53 mutations and prior venetoclax exposure, and a manageable safety profile. Under a Cooperative Research and Development Agreement (CRADA) with the National Cancer Institute (NCI), Actimab-A is being advanced across the NCI’s National Clinical Trials Network – which includes approximately 2,000 clinical trial sites through groups such as ECOG, SWOG, and Alliance – and is the subject of an ongoing frontline triplet combination trial with venetoclax and the hypomethylating agent ASTX-727 (Taiho Oncology) in newly diagnosed AML patients. Actimab-A is advancing toward a Phase 2/3 registrational program, with the goal of establishing Actimab-A as a foundational backbone therapy for patients with AML, myelodysplastic syndrome (MDS), and other CD33-expressing myeloid malignancies – a patient population that continues to face high unmet medical need.

(Press release, Actinium Pharmaceuticals, APR 22, 2026, View Source [SID1234664696])

Actinium Pharmaceuticals, Inc. Announces Compelling Pan-Tumor Data for ATNM-400 Demonstrating Broad Efficacy Across Prostate, Lung, and Breast Cancer Models at the 2026 American Association of Cancer Research Annual Meeting

On April 22, 2026 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, reported preclinical results for ATNM-400 across prostate, lung, and breast cancer models presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in San Diego, CA. ATNM-400 is a novel, first-in-class targeted radiotherapy utilizing the Actinium-225 (Ac-225) radioisotope that targets a non-PSMA membrane antigen overexpressed in advanced and therapy-refractory solid tumors across multiple oncology indications.

ATNM-400 is a novel, first-in-class targeted radiotherapy whose differentiation stems from both its target and its isotope. The target is a non-PSMA membrane antigen associated with treatment resistance in advanced solid tumors that is overexpressed across prostate cancer, non-small cell lung cancer (NSCLC), and breast cancer, and is further upregulated following treatment with standard-of-care therapies — providing a strong mechanistic rationale for ATNM-400 in the treatment-resistant disease settings that represent the greatest unmet need, and for combination regimens designed to exploit this treatment-induced target upregulation. The isotope, Actinium-225 (Ac-225), is a potent alpha emitter that, compared to beta emitters such as Lu-177, delivers high-energy radiation capable of inducing irreversible double-stranded DNA breaks, with a shorter path length that may limit off-target effects and enhance therapeutic precision. Together, this target-and-isotope combination positions ATNM-400 to overcome conventional resistance pathways and deliver durable tumor control while potentially avoiding toxicities such as interstitial lung disease that limit the use of antibody-drug conjugates — expanding the population of patients who could benefit from treatment.

Key Data and Highlights From the ATNM-400 AACR (Free AACR Whitepaper) Presentation

New preclinical data support ATNM-400 as a differentiated Ac-225 radioconjugate with potential applicability across multiple high-value solid tumor indications. ATNM-400 demonstrates a favorable tolerability profile, with no significant toxicity observed at therapeutic doses; and additionally:

In Prostate Cancer

Demonstrates in vivo efficacy across prostate cancer models with low, medium, and high PSMA expression, including PSMA-negative models.
Shows superior anti-tumor efficacy versus vehicle control, unconjugated antibody, and 177Lu–PSMA-617 (active ingredient in PLUVICTO) in both high -PSMA, (C4-2) and low (22Rv1) PSMA-expressing models, addressing both patients unlikely to respond to PSMA-targeted radioligand therapy (low-PSMA, 22Rv1) and those who relapse on it (C4-2).
Activity in PSMA-negative (DU145) models supports a differentiated profile, suggesting ATNM-400 could address mCRPC patients who are ineligible for or have progressed on PSMA-targeted radioligand therapy due to low or absent PSMA expression— a population with no currently approved targeted radiotherapy option.

In Lung Cancer

New data in the NCI-H1975 EGFR-mutant NSCLC model – a clinically relevant model of osimertinib-resistant disease – shows ATNM-400 as monotherapy or in combination with osimertinib exceeds the tumor growth inhibition of osimertinib plus chemotherapy, the current standard of care in post-osimertinib progression. These results extend the Company’s prior data demonstrating 100% complete tumor regression with the ATNM-400 plus osimertinib combination.
ATNM-400 monotherapy demonstrates greater anti-tumor activity than Dato-DXd (TROP-2 ADC approved in EGFR-mutant lung cancer) and izalontamab brengitecan (HER3-EGFR bispecific ADC in development for EGFR-mutant lung cancer). ATNM-400 also demonstrates greater anti-tumor activity than the EGFR-cMET bispecific antibody amivantamab (RYBREVANT) as shown in prior studies.

In Breast Cancer

New head-to-head data in the BT474 Clone-5 trastuzumab-resistant HER2+ breast cancer model which is a clinically relevant model of the post-trastuzumab setting, where treatment options are limited, demonstrate that ATNM-400, both as monotherapy and in combination with trastuzumab deruxtecan, achieves anti-tumor activity comparable to the approved HER2-ADC trastuzumab deruxtecan (ENHERTU). These results extend the Company’s SABCS 2025 data and position ATNM-400 as a potential alternative for patients who cannot tolerate HER2 ADCs due to interstitial lung disease, a known class-related toxicity.

In the same post-trastuzumab failure setting, ATNM-400 produces durable tumor growth inhibition after treatment discontinuation which exceeds both vehicle control and trastuzumab deruxtecan, supporting the potential for less frequent dosing and more durable disease control than ADCs.Sandesh Seth, Actinium’s Chairman and CEO, said, "The data we presented at AACR (Free AACR Whitepaper) are an important new piece of a much larger picture for ATNM-400. As a single agent, ATNM-400 continues to demonstrate activity across prostate, lung, and breast cancer in the treatment-resistant settings that represent the greatest unmet need, and also in combinations which can expand the available opportunity to additional patient populations. These data build on our previously disclosed results showing significant tumor regression when ATNM-400 is combined with osimertinib in EGFR-mutant lung cancer, and when combined with enzalutamide in prostate cancer, with similar combination potential emerging in breast cancer. What is becoming increasingly clear is that ATNM-400’s target antigen is upregulated by standard-of-care therapies, which creates a strong mechanistic rationale for ATNM-400 to rescue patients who progress approved agents and also to extend the benefit of these approved agents through combinations. We look forward to continuing to advance ATNM-400 toward the clinic with additional data to come in 2026."

The ATNM-400 AACR (Free AACR Whitepaper) presentation is available for viewing on the Presentations & Webinars page of Actinium’s website HERE.

Title: Preclinical Development of ATNM-400, a First-in-Class Actinium-225 Radioconjugate with Pan-Tumor Efficacy in Solid Tumors

Abstract Number: 5824

(Press release, Actinium Pharmaceuticals, APR 22, 2026, View Source [SID1234664695])