CalciMedica (Nasdaq: CALC) raises $15M, maps PAH and PH trial plans
Rhea-AI Filing Summary
CalciMedica, Inc. entered a securities purchase agreement for a private placement of 18,673,429 units, providing approximately $15 million in upfront gross proceeds and up to about $49 million in total potential gross proceeds including Series A and Series B warrant exercises.
Each unit includes common stock or a pre-funded warrant plus rights to Series A and B warrants, with exercise prices of $0.8033 and $1.00 per share, respectively. The company plans to use the funds to advance a pulmonary hypertension program, including a Phase 1b Auxora proof-of-concept study in PAH and IND-enabling work for oral candidate CM5480.
The company estimates that net proceeds, together with existing cash, will fund operations into the second half of 2027. CalciMedica also reported that the FDA reviewed a protocol amendment and interim safety data for the Phase 2 KOURAGE trial of Auxora in acute kidney injury and provided no comments, allowing dosing in the study to continue.
Positive
- None.
Negative
- None.
Insights
CALC secures structured financing and key FDA clarity to fund its PH strategy into 2027.
CalciMedica arranged a private placement of 18.67 million units for about $15M upfront and up to roughly $49M if Series A and B warrants are fully exercised. Pricing around $0.8033 per unit and insider participation align the round with market rules and internal support.
The company plans to channel proceeds into its pulmonary hypertension program: a Phase 1b proof-of-concept study of Auxora in PAH with data expected around mid-2027, plus IND-enabling work for oral CRAC inhibitor CM5480 targeting IND clearance by mid-2027. Management guides that this cash extends runway into the second half of 2027, reducing near-term financing pressure.
On the regulatory side, the FDA reviewed a protocol amendment and interim safety data from the Phase 2 KOURAGE trial in AKI and issued no comments, confirming Auxora dosing may continue. While the trial had a prior mortality imbalance linked to baseline severity rather than observed toxicity, future outcomes, warrant exercises, and stockholder approval for the warrants remain key uncertainties for investors.
8-K Event Classification
Key Figures
Key Terms
private placement financial
pre-funded warrant financial
Series A Warrant financial
pulmonary arterial hypertension (PAH) medical
acute kidney injury (AKI) medical
Investigational New Drug application regulatory
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
FORM
CURRENT REPORT
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Item 1.01 Entry into a Material Definitive Agreement
On June 23, 2026, CalciMedica, Inc. (the “Company”) entered into a securities purchase agreement (the “Purchase Agreement”) with certain new and existing institutional and accredited investors named therein (each, an “Investor” and collectively, the “Investors”), for the private placement (the “Private Placement”) of an aggregate of 18,673,429 units (the “Units”), each Unit comprised of (i) (A) one share of the Company’s common stock, par value $0.0001 per share (the “Common Stock”), or (B) one pre-funded warrant to purchase one share of Common Stock (each, a “Pre-Funded Warrant” and collectively, the “Pre-Funded Warrants”), and, in each case, (ii) a right to receive one Series A warrant to purchase one share of Common Stock or a pre-funded warrant to purchase one share of Common Stock (each, a “Series A Warrant” and collectively, the “Series A Warrants”) upon receipt of Stockholder Approval (as defined below), and (iii) a right to receive one Series B warrant to purchase one share of Common Stock or a pre-funded warrant to purchase one share of Common Stock (each, a “Series B Warrant” and collectively, the “Series B Warrants”, and together with the Series A Warrants, the “Warrants”) upon receipt of Stockholder Approval (the shares of Common Stock issuable upon exercise of the Pre-Funded Warrants and Warrants, the “Warrant Shares”). “Stockholder Approval” means such approval as may be required by the applicable rules and regulations of The Nasdaq Capital Market from the stockholders of the Company with respect to the issuance of all of the Series A Warrants and Series B Warrants and the Warrant Shares issuable upon the exercise thereof. A Unit comprised of one share of Common Stock, one right to receive a Series A Warrant and one right to receive a Series B Warrant shall have a purchase price of $0.8033 (the “Common Stock Unit Purchase Price”) and a Unit comprised of one Pre-Funded Warrant, one right to receive a Series A Warrant and one right to receive a Series B Warrant shall have a purchase price of $0.8032 (the “Pre-Funded Warrant Unit Purchase Price”, and together with the Common Stock Unit Purchase Price, the “Purchase Prices”). Rachel Leheny, Ph.D., the Company’s Chief Executive Officer, a member of the board of directors of the Company (the “Board”) and a beneficial owner of more than 5% of the Company’s common stock, Eric Roberts, the Company’s Chief Business Officer, a member of the Board and a beneficial owner of more than 5% of the Company’s common stock, Sudarshan Hebbar, M.D., the Company’s Chief Medical Officer, Robert Wilson, a member of the Board, Sanderling Venture Partners VI Co-Investment Fund, L.P., a beneficial owner of more than 5% of the Company’s common stock and an affiliate of Fred Middleton, a member of the Board, Alafi Capital Company, LLC, a beneficial owner of more than 5% of the Company’s common stock, and Bering Partners II, L.P., a beneficial owner of more than 5% of the Company’s common stock, are participating in the Private Placement for an aggregate of 6,908,996 Units. The Purchase Prices for each Unit, as applicable, for any Investor that is an officer, director, employee or consultant of the Company was priced above the Nasdaq Consolidated Closing Bid Price as of June 23, 2026.
The upfront gross proceeds for the Private Placement are expected to be approximately $15.0 million, before deducting placement agent fees and other expenses, and up to approximately an additional $34 million in gross proceeds if the Warrants are fully exercised for cash. The closing of the Private Placement is expected to occur on or about June 25, 2026, subject to the satisfaction of customary closing conditions. The Private Placement is being conducted in accordance with applicable rules of The Nasdaq Stock Market LLC.
Guggenheim Securities, LLC is acting as the sole placement agent for the Private Placement. The Company has agreed to pay the placement agent customary placement fees in its capacity as placement agent for the sale of the Units to the Investors.
The Company expects to use the net proceeds from the Private Placement to fund research and development of its product candidates, working capital and general corporate purposes.
Each Pre-Funded Warrant will have an exercise price of $0.0001 per Pre-Funded Warrant Share, will be immediately exercisable on the date of issuance and will not expire. If a registration statement covering the resale of the Pre-Funded Warrant Shares is not available, the Pre-Funded Warrants may also be exercisable on a net exercise “cashless” basis. The Pre-Funded Warrants may not be exercised if the aggregate number of shares of Common Stock beneficially owned by the holder thereof immediately following such exercise would exceed a specified beneficial ownership limitation, not to exceed 19.99%.
The Series A Warrants shall have an exercise price equal to $0.8033 per Warrant Share, will be exercisable immediately upon issuance and will expire on the earlier of (i) 18 months after the closing date of the Private Placement and (ii) 30 days following the Company’s public announcement of the clearance of its Investigational New Drug Application by the U.S. Food and Drug Administration for CM5480 (the “Series A Expiration Date”); provided that if such date occurs prior to the date on which Stockholder Approval is obtained (the “Stockholder Approval Date”), the Series A Expiration Date shall be extended until 30 days following the Stockholder Approval Date. The Series A Warrants will be issued upon receipt of Stockholder Approval. If a registration statement covering the resale of the Warrant Shares is not available, the Series A Warrants may also
be exercisable on a net exercise “cashless” basis. The Series A Warrants may not be exercised if the aggregate number of shares of Common Stock beneficially owned by the holder thereof immediately following such exercise would exceed a specified beneficial ownership limitation, not to exceed 19.99%. To the extent that exercise of the Series A Warrants will result in a holder thereof beneficially owning shares of Common Stock above such ownership limitations, the holder may exercise its Series A Warrants for pre-funded warrants to purchase shares of Common Stock. Such pre-funded warrants will have terms substantially similar to the Pre-Funded Warrants described above.
The Series B Warrants shall have an exercise price equal to $1.00 per Warrant Share, will be exercisable immediately upon issuance and will expire five years from the closing date of the Private Placement. The Series B Warrants will be issued upon receipt of Stockholder Approval. If a registration statement covering the resale of the Warrant Shares is not available, the Series B Warrants may also be exercisable on a net exercise “cashless” basis. The Series B Warrants may not be exercised if the aggregate number of shares of Common Stock beneficially owned by the holder thereof immediately following such exercise would exceed a specified beneficial ownership limitation, not to exceed 19.99%. To the extent that exercise of the Series B Warrants will result in a holder thereof beneficially owning shares of Common Stock above such ownership limitations, the holder may exercise its Series B Warrants for pre-funded warrants to purchase shares of Common Stock. Such pre-funded warrants will have terms substantially similar to the Pre-Funded Warrants described above.
The exercise price and the number of Warrant Shares will be subject to appropriate adjustment in the event of certain stock dividends and distributions, stock splits, stock combinations, reclassifications or similar events affecting the Common Stock.
In the event of certain fundamental transactions (as described in the respective warrants), (i) a holder of Pre-Funded Warrants or Series A Warrants will have the right to receive, upon exercise, the same amount and kind of securities, cash or property that such holder would have received had they exercised in full immediately prior to such fundamental transaction, without regard to any limitations on exercise, and (ii) a holder of Series B Warrants will have the right, at its election, to receive a cash payment equal to the Black Scholes value of the remaining unexercised portion of such Series B Warrants in lieu of the foregoing, calculated in accordance with the terms of the Series B Warrants.
Pursuant to the Purchase Agreement, the Company agreed to file a registration statement with the U.S. Securities and Exchange Commission (the “SEC”) within 30 days after the closing of the Private Placement (subject to certain exceptions) for purposes of registering the resale of the shares of Common Stock and the Warrant Shares, to use its reasonable best efforts to have such registration statement declared effective within the time period set forth in the Purchase Agreement, and to keep such registration statement effective until the earliest of (i) the time as all of the shares of Common Stock and Warrant Shares purchased by the Investors pursuant to the terms of the Purchase Agreement have been sold or otherwise transferred by the holder thereof pursuant to and in a manner contemplated by the registration statement, (ii) such time as such shares of Common Stock or Warrant Shares are sold pursuant to Rule 144 under circumstances in which any legend borne by such security relating to restrictions on transferability thereof, under the Securities Act of 1933, as amended (the “Securities Act”), or otherwise, is removed by the Company, or (iii) such time as the shares of Common Stock and Warrant Shares become eligible for resale by non-affiliates without any volume limitations or other restrictions pursuant to Rule 144 under the Securities Act or any other rule of similar effect.
The Purchase Agreement contains customary representations, warranties and covenants that were made solely for the benefit of the parties to the Purchase Agreement. Such representations, warranties and covenants (i) are intended as a way of allocating risk between the parties to the Purchase Agreement and not as statements of fact and (ii) may apply standards of materiality in a way that is different from what may be viewed as material by stockholders of, or other investors in, the Company. Accordingly, the Purchase Agreement is included with this filing only to provide investors with information regarding the terms of the transaction and not to provide investors with any other factual information regarding the Company. Investors should not rely on the representations, warranties and covenants or any descriptions thereof as characterizations of the actual state of facts or condition of the Company or any of its subsidiaries or affiliates. Moreover, information concerning the subject matter of the representations and warranties may change after the date of the Purchase Agreement, which subsequent information may or may not be fully reflected in public disclosures. Additionally, the Purchase Agreement contains customary indemnification obligations of the Company and the Investors, including for liabilities under the Securities Act, and other obligations of the parties.
The foregoing descriptions of the Purchase Agreement, Pre-Funded Warrant, Series A Warrant and Series B Warrant do not purport to be complete and are qualified in their entirety by reference to the form of Purchase Agreement, form of Pre-Funded Warrant, form of Series A Warrant and form of Series B Warrant, which are filed as Exhibit 10.1, Exhibit 4.1, Exhibit 4.2 and Exhibit 4.3, respectively, to this Current Report on Form 8-K and incorporated herein by reference.
Item 3.02 Unregistered Sales of Equity Securities
The disclosures set forth in Item 1.01 above are incorporated by reference into this Item 3.02.
The securities described above under Item 1.01 have not been registered under the Securities Act of 1933, as amended (“Securities Act”), or any state securities laws. The Company is relying on the exemption from the registration requirements of the Securities Act by virtue of Section 4(a)(2) thereof. The Investors provided representations appropriate for a private placement of securities. The securities were offered without any general solicitation by the Company or its representatives. Restrictive legends will be affixed to the securities issued in the Private Placement.
Neither this Current Report on Form 8-K nor any exhibit attached hereto is an offer to sell or the solicitation of an offer to buy shares of Common Stock or other securities of the Company.
Item 7.01 Regulation FD Disclosure
On June 24, 2026, the Company issued a press release announcing an update on its interactions with the U.S. Food and Drug Administration (“FDA”). A copy of the press release is attached as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated herein by reference.
On June 24, 2026, the Company issued a press release announcing that it has entered into the Purchase Agreement and provided other business updates. A copy of the press release is attached as Exhibit 99.2 to this Current Report on Form 8-K and is incorporated herein by reference.
The Company estimates, based on its current operating plan, that the net proceeds from the Private Placement, together with its current cash and cash equivalents (but excluding any additional proceeds that may be received upon the exercise of Series A Warrants or Series B Warrants), will be sufficient to fund its operations into the second half of 2027.
Included as Exhibit 99.3 to this Form 8-K is a slide presentation titled “Investor Update” dated June 2026, that is incorporated herein by reference. The Company intends to utilize this presentation and its contents in various meetings with securities analysts, investors and others.
The information in this Item 7.01 of this Current Report on Form 8-K, including the attached Exhibits 99.1, 99.2 and 99.3, is being furnished and shall not be deemed “filed” for the purposes of Section 18 of the Securities Exchange Act of 1934, as amended, or otherwise subject to the liabilities of that section or Sections 11 and 12(a)(2) of the Securities Act of 1933, as amended. The information contained in this Item 7.01, including Exhibits 99.1, 99.2, and 99.3, shall not be incorporated by reference into any filing we make with the SEC whether before or after the date hereof, regardless of any general incorporation language in such filing.
Item 8.01 Other Events
Company Update
On June 24, 2026, the Company announced that it intends to use the proceeds of the Private Placement to advance a focused pulmonary hypertension (“PH”) strategy built on its CRAC channel inhibition platform. The Company plans to conduct a capital-efficient Phase 1b proof-of-concept study evaluating Auxora™, its intravenous CRAC channel inhibitor, in patients with pulmonary arterial hypertension (“PAH”), with data anticipated mid-2027. This study is intended to generate early human evidence for CRAC channel inhibition in PH and de-risk the development of CM5480, the Company’s proprietary oral CRAC channel inhibitor candidate for chronic treatment, for which Investigational New Drug (“IND”) application clearance is anticipated in mid-2027. Proceeds are also expected to support continued IND-enabling activities for CM5480 and general corporate purposes.
PH includes a diverse group of diseases, but progressive right ventricular dysfunction is a shared consequence and a key determinant of survival across disease groups. Orai1, the pore-forming subunit of the CRAC channel, is upregulated in diseased pulmonary vasculature and cardiac tissue, where persistent CRAC channel signaling has been linked to proliferation, inflammation, vasoconstriction, fibrosis, and remodeling. In preclinical PH models, CM5480 and other CRAC channel inhibitors have been observed to reduce pulmonary vascular resistance, improve cardiac output, reduce right ventricular hypertrophy and fibrosis, and improve left ventricular function. In a rodent pulmonary artery banding model, which isolates cardiac effects from pulmonary vascular effects, CRAC channel inhibition with CM5480 also demonstrated evidence of direct protective activity in the right ventricle.
The planned Auxora Phase 1b study is designed to deliver an early, capital-efficient clinical signal on CRAC channel inhibition in PH. Auxora has been evaluated in more than 350 patients across completed and ongoing clinical trials. Following the Company’s pause of enrollment in the Phase 2 KOURAGE trial of Auxora in acute kidney injury (“AKI”), comprehensive internal and external safety reviews identified no evidence of drug-related toxicity. The Company subsequently submitted a protocol amendment and interim safety data to the FDA, and the agency completed its review without comments or questions, allowing clinical development of Auxora to proceed. The Company believes Auxora’s established safety profile supports its continued development across the PH program and other indications.
FDA Update
On June 24, 2026, the Company announced that the FDA has reviewed a protocol amendment and interim safety data for the Company’s Phase 2 KOURAGE trial in patients with Stage 2 or Stage 3 AKI with associated acute hypoxemic respiratory failure (“AHRF”). Following the applicable review period, the Company has received no comments from the FDA on the submission, meaning that the Company may continue to dose patients with Auxora™ in the study.
As previously disclosed, in January 2026, the Company announced a pause in enrollment for the Phase 2 KOURAGE trial following a recommendation from the trial’s Independent Data Monitoring Committee (the “IDMC”) regarding a safety concern relating to a mortality imbalance that warranted reevaluation of the study design. The IDMC did not identify evidence of drug-related toxicity, and the Company’s comprehensive review, performed in conjunction with external experts, reached the same conclusion while identifying imbalances in patients’ baseline disease severity that necessitated revisions to the protocol design.
In March 2026, the Company submitted an amendment to the KOURAGE trial to address design issues, which included refinements to patient inclusion criteria and changes to stratification methodology. The submission included a comprehensive safety assessment of the 107 patients who were dosed prior to the pause in enrollment, including cause-of-death information for all deaths and an analysis of serious adverse events (“SAEs”). Based on the Company’s review, the observed SAEs were consistent with previous clinical experience with Auxora and did not appear to be drug related. The FDA has confirmed that the Clinical Pharmacology team of the Division of Cardiology and Nephrology has no comments regarding this submission. As the KOURAGE trial was never placed on clinical hold, and the decision to pause enrollment was made solely at the discretion of the Company, the FDA is not obligated to respond to the IND amendment. Following more than 60 days of review, the information contained in the amendment has resulted in no comments or questions from the FDA and no clinical hold communication.
The Company expects feedback from the FDA on the design of a potential pivotal program evaluating Auxora in acute pancreatitis in the third quarter of 2026.
Forward-Looking Statements
This Current Report on Form 8-K (this “Report”) contains forward-looking statements which include, but are not limited to, the Company’s statements regarding the timing, size, and completion of the proposed Private
Placement; the expected gross proceeds from the Private Placement, including any additional gross proceeds that may be received by the Company upon exercise, if any, of the Warrants that are issuable upon Stockholder Approval; the anticipated use of proceeds and expected cash runway; the Company’s planned and ongoing preclinical and clinical activities and their expected timing, including the planned Auxora Phase 1b study in PAH and the anticipated timing of data therefrom; the planned IND submission for CM5480 and the expected timing for clearance thereof; the potential of CRAC channel inhibition and of the Company’s product candidates to provide therapeutic benefit in PAH, PH, and other diseases; the expectation that the Phase 1b study of Auxora in PAH will be capital efficient and potentially generate early human evidence for CRAC channel inhibition in PH; the belief that CRAC channel inhibition has the potential to be the first therapy to provide direct right ventricular support and anti-remodeling activity; the Company’s expectation to receive feedback from the FDA regarding the design of a potential pivotal program evaluating Auxora in acute pancreatitis in the third quarter of 2026; and the Company’s belief that Auxora’s safety profile supports its continued development across the PH program and other indications. These forward-looking statements are subject to the safe harbor provisions under the Private Securities Litigation Reform Act of 1995. The Company’s expectations and beliefs regarding these matters may not materialize. Actual outcomes and results may differ materially from those contemplated by these forward-looking statements as a result of uncertainties, risks, and changes in circumstances, including but not limited to risks and uncertainties related to: the Company’s ability to satisfy the closing conditions of the Private Placement; the Company’s ability to obtain Stockholder Approval to issue the Warrants; even if the Warrants are issued the holders may never exercise such Warrants and the Company may not receive any additional proceeds therefrom; the impact of fluctuations in global financial markets on the Company’s business and the actions it may take in response thereto; the Company’s ability to execute its plans and strategies; the ability to obtain and maintain regulatory approval for Auxora and CM5480; results from clinical trials or preclinical studies may not be indicative of results that may be observed in the future; potential safety and other complications from Auxora and CM5480; the scope, progress and expansion of developing and commercializing Auxora and CM5480; the size and growth of the market therefor and the rate and degree of market acceptance thereof; economic, business, competitive, and/or regulatory factors affecting the business of the Company generally; the Company’s ability to protect its intellectual property position; the impact of government laws and regulations; and the Company’s financial position and need for additional capital. Additional risks and uncertainties that could cause actual outcomes and results to differ materially from those contemplated by the forward-looking statements are included under the caption “Risk Factors” in the Company’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2026, filed with the SEC on May 12, 2026, and elsewhere in the Company’s subsequent reports on Form 10-K, Form 10-Q or Form 8-K filed with the SEC from time to time and available at www.sec.gov. These documents can be accessed on the Company’s web page at ir.calcimedica.com/financials-filings/sec-filings. The forward-looking statements contained herein are made as of the date hereof, and the Company undertakes no obligation to update them after this date, except as required by law.
Item 9.01 Financial Statements and Exhibits
(d) Exhibits
| Exhibit No. |
Description | |
| 4.1 | Form of Pre-Funded Warrant | |
| 4.2 | Form of Series A Warrant | |
| 4.3 | Form of Series B Warrant | |
| 10.1 | Form of Securities Purchase Agreement, dated June 23, 2026, by and between CalciMedica, Inc. and each of the Investors party thereto | |
| 99.1 | Press Release dated June 24, 2026 | |
| 99.2 | Press Release, dated June 24, 2026 | |
| 99.3 | Investor Update, dated June 2026 | |
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document) | |
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, as amended, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| CalciMedica, Inc. | ||||||
| Date: June 24, 2026 | By: | /s/ A. Rachel Leheny, Ph.D. | ||||
| Name: | A. Rachel Leheny, Ph.D. | |||||
| Title: | Chief Executive Officer | |||||
Exhibit 99.1
CalciMedica Announces Clinical Development of Auxora May Proceed Following FDA Review of
KOURAGE Trial Interim Safety Data
FDA reviewed a protocol amendment and interim safety data from the KOURAGE trial evaluating Auxora
in AKI patients
No comments or questions were received
Confirms CalciMedica’s ability to continue clinical development of Auxora across indications
LA JOLLA, Calif., June 24, 2026 – CalciMedica, Inc. (“CalciMedica” or the “Company”) (Nasdaq: CALC), a clinical-stage biopharmaceutical company developing novel calcium release-activated calcium (CRAC) channel inhibition therapies for serious inflammatory, immunologic, and cardiopulmonary diseases, today announced that the U.S. Food and Drug Administration (FDA) has reviewed a protocol amendment and interim safety data for CalciMedica’s Phase 2 KOURAGE trial in patients with Stage 2 or Stage 3 acute kidney injury (AKI) with associated acute hypoxemic respiratory failure (AHRF). Following the applicable review period, the Company has received no comments from the FDA on the submission, meaning that CalciMedica may continue to dose patients with Auxora™ in the study.
In January 2026, CalciMedica announced a pause in enrollment for the Phase 2 KOURAGE trial following a recommendation from the trial’s Independent Data Monitoring Committee (IDMC) regarding a safety concern relating to a mortality imbalance that warranted reevaluation of the study design. The IDMC did not identify evidence of drug-related toxicity, and the Company’s comprehensive review, performed in conjunction with external experts, reached the same conclusion while identifying imbalances in patients’ baseline disease severity that necessitated revisions to the protocol design.
In March 2026, CalciMedica submitted an amendment to the KOURAGE trial to address design issues, which included refinements to patient inclusion criteria and changes to stratification methodology. The submission included a comprehensive safety assessment of the 107 patients who were dosed prior to the pause in enrollment, including cause-of-death information for all deaths and an analysis of serious adverse events (SAEs). Based on the Company’s review, the observed SAEs were consistent with previous clinical experience with Auxora and did not appear to be drug related. The FDA has confirmed that the Clinical Pharmacology team of the Division of Cardiology and Nephrology has no comments regarding this submission. As the KOURAGE trial was never placed on clinical hold, and the decision to pause enrollment was made solely at the discretion of the Company, the FDA is not obligated to respond to the IND amendment. Following more than 60 days of review, the information contained in the amendment has resulted in no comments or questions from the FDA and no clinical hold communication.
CalciMedica expects feedback from the FDA on the design of a potential pivotal program evaluating Auxora in acute pancreatitis in the third quarter of 2026.
1
About CalciMedica
CalciMedica is a clinical-stage biopharmaceutical company developing novel calcium release-activated calcium (CRAC) channel inhibition therapies for inflammatory, immunologic, and cardiopulmonary diseases. The Company’s pipeline includes Auxora™ (zegocractin), its intravenous CRAC channel inhibitor, and CM5480, its proprietary, selective oral CRAC channel inhibitor candidate. Auxora has been evaluated in more than 350 patients across completed and ongoing clinical trials and is planned to be evaluated in a Phase 1b proof-of-concept study in patients with pulmonary arterial hypertension (PAH). CM5480 is being developed as a potential chronic oral therapy for chronic inflammatory diseases such as pulmonary hypertension (PH), with IND clearance expected in mid-2027. Together, the programs are intended to establish CRAC channel inhibition as a differentiated therapeutic approach targeting both pulmonary vascular remodeling and right ventricular dysfunction in PH. For more information, please visit www.calcimedica.com.
Forward-Looking Statements This communication contains forward-looking statements which include, but are not limited to, statements regarding CalciMedica’s clinical development plans for Auxora™, including in acute kidney injury and acute pancreatitis; CalciMedica’s ability to continue dosing patients with Auxora in the KOURAGE trial or otherwise continue clinical development of Auxora following FDA review of the KOURAGE protocol amendment and interim safety data; CalciMedica’s interpretation of the FDA’s lack of comments or questions regarding the submission; the potential resumption, continuation, design, conduct, timing, enrollment or completion of the KOURAGE trial or any future clinical trial evaluating Auxora in AKI; the potential safety, efficacy, clinical utility and regulatory development path for Auxora; CalciMedica’s expectation to receive feedback from FDA regarding the design of a potential pivotal program evaluating Auxora in acute pancreatitis in the third quarter of 2026; CalciMedica’s plans to advance CM5480 as a potential oral therapy for PH; and the potential of CalciMedica’s proprietary technology to provide therapeutic benefits in inflammatory, immunologic and cardiopulmonary diseases. These forward-looking statements are subject to the safe harbor provisions under the Private Securities Litigation Reform Act of 1995. CalciMedica’s expectations and beliefs regarding these matters may not materialize. Actual outcomes and results may differ materially from those contemplated by these forward-looking statements as a result of uncertainties, risks, and changes in circumstances, including but not limited to risks and uncertainties related to: the impact of fluctuations in global financial markets on CalciMedica’s business and the actions it may take in response thereto; CalciMedica’s ability to execute its plans and strategies; the ability to obtain and maintain regulatory approval for Auxora and CM5480; results from clinical trials or preclinical studies may not be indicative of results that may be observed in the future; potential safety and other complications from Auxora and CM5480; the scope, progress and expansion of developing and commercializing Auxora; the size and growth of the market therefor and the rate and degree of market acceptance thereof; economic, business, competitive, and/or regulatory factors affecting the business of CalciMedica generally; CalciMedica’s ability to protect its intellectual property position; the impact of government laws and regulations; and CalciMedica’s financial position and need for additional capital. Additional risks and uncertainties that could cause actual outcomes and results to differ materially from those contemplated by the forward-looking statements are included under the caption “Risk Factors” in CalciMedica’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2026, filed with the SEC on May 12, 2026, and elsewhere in CalciMedica’s subsequent reports on Form 10-K, Form 10-Q or Form 8-K filed
2
with the SEC from time to time and available at www.sec.gov. These documents can be accessed on CalciMedica’s web page at ir.calcimedica.com/financials-filings/sec-filings. The forward-looking statements contained herein are made as of the date hereof, and CalciMedica undertakes no obligation to update them after this date, except as required by law.
Contact Information
Kevin Murphy
calcimedica@argotpartners.com
(212) 600-1902
3
Exhibit 99.2
CalciMedica Announces Private Placement Financing for Up to Approximately $49 Million to Advance Pulmonary Hypertension Program
Proceeds expected to support a focused pulmonary hypertension strategy, including a Phase 1b proof-of-concept study evaluating Auxora™ in PAH, with data anticipated mid-2027, and advancement of oral CRAC channel inhibitor CM5480 to IND clearance expected mid-2027
Anticipated cash runway into 2H 2027 with upfront proceeds
LA JOLLA, Calif., June 24, 2026 – CalciMedica Inc. (“CalciMedica” or the “Company”) (Nasdaq: CALC), a clinical-stage biopharmaceutical company developing novel calcium release-activated calcium (CRAC) channel inhibition therapies for serious inflammatory, immunologic, and cardiopulmonary diseases, today announced it has entered into a definitive securities purchase agreement with leading healthcare investors for a private placement for up to approximately $49 million in gross proceeds.
The financing includes participation from new and existing investors, including members of CalciMedica’s Board of Directors and management team. In the private placement, the Company will sell an aggregate of 18,673,429 units, with each unit comprised of (i) one share of its common stock or one pre-funded warrant to purchase shares of common stock at an exercise price of $0.0001 per share, (ii) a right to receive one Series A warrant to purchase shares of its common stock or pre-funded warrants to purchase shares of its common stock at an exercise price of $0.8033 per share, and (iii) a right to receive one Series B warrant to purchase shares of its common stock or pre-funded warrants to purchase shares of its common stock at an exercise price of $1.00 per share. The private placement is comprised of (i) upfront gross proceeds of approximately $15 million, representing a purchase price of $0.8033 for each unit or $0.8032 for each unit including a pre-funded warrant sold in lieu of common stock), (ii) Series A warrants with the potential for up to an additional $15 million in gross proceeds if exercised in full, and (iii) Series B warrants with the potential for up to approximately an additional $19 million in gross proceeds if exercised in full. Both Series A warrants and Series B warrants are issuable subject to stockholder approval in accordance with Nasdaq listing rules. The purchase price for each unit for the members of CalciMedica’s Board of Directors and management team will be priced at or above the Nasdaq Consolidated Closing Bid Price as of June 23, 2026.
CalciMedica intends to use the proceeds to advance a focused pulmonary hypertension (PH) strategy built on its CRAC channel inhibition platform. The Company plans to conduct a capital-efficient Phase 1b proof-of-concept study evaluating Auxora™, its intravenous CRAC channel inhibitor, in patients with pulmonary arterial hypertension (PAH), with data anticipated mid-2027. This study is intended to generate early human evidence for CRAC channel inhibition in PH and de-risk the development of CM5480, the Company’s proprietary oral CRAC channel inhibitor candidate for chronic treatment, for which IND clearance is anticipated in mid-2027. Proceeds are also expected to support continued IND-enabling activities for CM5480 and general corporate purposes.
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“This financing reflects strong validation from leading biotech investors of our strategy to develop a differentiated, mechanistically novel therapy for patients with pulmonary hypertension, where PAH represents an established multi-billion-dollar market and significant unmet need remains across the broader pulmonary hypertension spectrum,” said Rachel Leheny, Ph.D., Chief Executive Officer of CalciMedica. “Right ventricular failure is the principal driver of morbidity and mortality across PH, yet approved therapies act primarily on the pulmonary vasculature. CRAC channel inhibition has shown activity in both the pulmonary vasculature and the heart in preclinical models, and we believe it has the potential to be the first therapy to provide direct right ventricular support and anti-remodeling activity. With this capital, we expect to generate human proof-of-concept data with Auxora while advancing our oral candidate, CM5480, into the clinic.”
PH includes a diverse group of diseases, but progressive right ventricular dysfunction is a shared consequence and a key determinant of survival across disease groups. Orai1, the pore-forming subunit of the CRAC channel, is upregulated in diseased pulmonary vasculature and cardiac tissue, where persistent CRAC channel signaling has been linked to proliferation, inflammation, vasoconstriction, fibrosis, and remodeling. In preclinical PH models, CM5480 and other CRAC channel inhibitors have been observed to reduce pulmonary vascular resistance, improve cardiac output, reduce right ventricular hypertrophy and fibrosis, and improve left ventricular function. In a rodent pulmonary artery banding model, which isolates cardiac effects from pulmonary vascular effects, CRAC channel inhibition with CM5480 also demonstrated evidence of direct protective activity in the right ventricle.
The planned Auxora Phase 1b study is designed to deliver an early, capital-efficient clinical signal on CRAC channel inhibition in PH. Auxora has been evaluated in more than 350 patients across completed and ongoing clinical trials. Following the Company’s pause of enrollment in the Phase 2 KOURAGE trial of Auxora in acute kidney injury (AKI), comprehensive internal and external safety reviews identified no evidence of drug-related toxicity. CalciMedica subsequently submitted a protocol amendment and interim safety data to the FDA, and the agency completed its review without comments or questions, allowing clinical development of Auxora to proceed. The Company believes Auxora’s established safety profile supports its continued development across the PH program and other indications.
“The preclinical animal model and genetic expression data supporting CRAC channel inhibition in pulmonary hypertension are compelling, particularly given the evidence of direct effects on cardiac function and right ventricular remodeling and failure,” said Sudarshan Hebbar, M.D., Chief Medical Officer of CalciMedica. “Auxora’s safety database allows us to move directly into a focused proof-of-concept design in PAH with hemodynamic and imaging endpoints. A positive signal would both establish Auxora’s potential in hospitalized PH settings and potentially de-risk our oral chronic-dosing program with CM5480.”
Guggenheim Securities, LLC is acting as sole placement agent in connection with the private placement financing.
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The offer and sale of the foregoing securities are being made in a transaction not involving a public offering and the securities to be sold in the private placement have not been registered under the Securities Act of 1933, as amended (Securities Act), or any state or other applicable jurisdiction’s securities laws, and may not be offered or sold in the United States absent registration or an applicable exemption from the registration requirements of the Securities Act and applicable state or other jurisdictions’ securities laws. Pursuant to the securities purchase agreement, the Company has agreed to file a registration statement with the U.S. Securities and Exchange Commission (SEC) registering the resale of the shares of common stock issued in the private placement and the shares of common stock issuable upon the exercise of the pre-funded warrants, the Series A warrants (including upon exercise of any pre-funded warrants issued upon exercise of the Series A warrants), and the Series B warrants (including upon exercise of any pre-funded warrants issued upon exercise of the Series B warrants) issued in the private placement no later than the 30th day after the closing of the private placement.
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 offer, solicitation or sale of these securities in any jurisdiction in which such offer, solicitation or sale would be unlawful. Any offering of the securities under the resale registration statement will only be made by means of a prospectus.
About CM5480 and Auxora
CM5480 is CalciMedica’s proprietary, selective, oral CRAC channel inhibitor candidate in preclinical development for chronic inflammatory diseases, with the potential to be a first-in-class, differentiated therapy targeting pulmonary vascular and right ventricular remodeling — key drivers of disease progression in PH. Auxora™ (zegocractin) is CalciMedica’s intravenous CRAC channel inhibitor, which has been evaluated in more than 350 patients across completed and ongoing clinical trials in acute pancreatitis, severe COVID-19 pneumonia, and acute kidney injury.
About CalciMedica
CalciMedica is a clinical-stage biopharmaceutical company developing novel calcium release-activated calcium (CRAC) channel inhibition therapies for inflammatory, immunologic, and cardiopulmonary diseases. The Company’s pipeline includes Auxora™ (zegocractin), its intravenous CRAC channel inhibitor, and CM5480, its proprietary, selective oral CRAC channel inhibitor candidate. Auxora has been evaluated in more than 350 patients across completed and ongoing clinical trials and is planned to be evaluated in a Phase 1b proof-of-concept study in patients with pulmonary arterial hypertension (PAH). CM5480 is being developed as a potential chronic oral therapy for chronic inflammatory diseases such as pulmonary hypertension (PH), with IND clearance expected in mid-2027. Together, the programs are intended to establish CRAC channel inhibition as a differentiated therapeutic approach targeting both pulmonary vascular remodeling and right ventricular dysfunction in PH. For more information, please visit www.calcimedica.com.
Forward-Looking Statements
This communication contains forward-looking statements which include, but are not limited to, CalciMedica’s statements regarding the timing, size, and completion of the proposed private placement; the expected gross proceeds from the private placement, including any additional gross proceeds that may be received by the Company upon exercise, if any, of the warrants that are issuable upon stockholder approval; the anticipated use of proceeds and expected cash runway; CalciMedica’s
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planned and ongoing preclinical and clinical activities and their expected timing, including the planned Auxora Phase 1b study in PAH and the anticipated timing of data therefrom; the planned IND submission for CM5480 and the expected timing for clearance thereof; the potential of CRAC channel inhibition and of CalciMedica’s product candidates to provide therapeutic benefit in PAH, PH, and other diseases; the expectation that the Phase 1b study of Auxora in PAH will be capital efficient and potentially generate early human evidence for CRAC channel inhibition in PH; the belief that CRAC channel inhibition has the potential to be the first therapy to provide direct right ventricular support and anti-remodeling activity; and the Company’s belief that Auxora’s safety profile supports its continued development across the PH program and other indications. These forward-looking statements are subject to the safe harbor provisions under the Private Securities Litigation Reform Act of 1995. CalciMedica’s expectations and beliefs regarding these matters may not materialize. Actual outcomes and results may differ materially from those contemplated by these forward-looking statements as a result of uncertainties, risks, and changes in circumstances, including but not limited to risks and uncertainties related to: CalciMedica’s ability to satisfy the closing conditions of the private placement; the Company’s ability to obtain stockholder approval to issue the warrants; even if the warrants are issued the holders may never exercise such warrants and CalciMedica may not receive any additional proceeds therefrom; the impact of fluctuations in global financial markets on CalciMedica’s business and the actions it may take in response thereto; CalciMedica’s ability to execute its plans and strategies; the ability to obtain and maintain regulatory approval for Auxora and CM5480; results from clinical trials or preclinical studies may not be indicative of results that may be observed in the future; potential safety and other complications from Auxora and CM5480; the scope, progress and expansion of developing and commercializing Auxora and CM5480; the size and growth of the market therefor and the rate and degree of market acceptance thereof; economic, business, competitive, and/or regulatory factors affecting the business of CalciMedica generally; CalciMedica’s ability to protect its intellectual property position; the impact of government laws and regulations; and CalciMedica’s financial position and need for additional capital. Additional risks and uncertainties that could cause actual outcomes and results to differ materially from those contemplated by the forward-looking statements are included under the caption “Risk Factors” in CalciMedica’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2026, filed with the SEC on May 12, 2026, and elsewhere in CalciMedica’s subsequent reports on Form 10-K, Form 10-Q or Form 8-K filed with the SEC from time to time and available at www.sec.gov. These documents can be accessed on CalciMedica’s web page at ir.calcimedica.com/financials-filings/sec-filings. The forward-looking statements contained herein are made as of the date hereof, and CalciMedica undertakes no obligation to update them after this date, except as required by law.
Contact Information
Kevin Murphy
calcimedica@argotpartners.com
(212) 600-1902
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Investor Update June 2026 Exhibit 99.3
Forward-Looking Statements This presentation contains forward-looking statements which include, but are not limited to, statements regarding CalciMedica’s business strategy and clinical development plans; the design and potential benefits of CalciMedica’s product candidates; CalciMedica’s ongoing and planned clinical trials; expected Intellectual Property (IP) protections; the timing for CalciMedica’s receipt and announcement of data from its clinical trials and other clinical and regulatory milestones, including expectations regarding the timing for regulatory approvals; the estimated patient populations and addressable market for CalciMedica’s product candidates; and expectations regarding CalciMedica’s financial position, capital requirements, and anticipated cash runway. These forward-looking statements are subject to the safe harbor provisions under the Private Securities Litigation Reform Act of 1995. CalciMedica’s expectations and beliefs regarding these matters may not materialize. Actual outcomes and results may differ materially from those contemplated by these forward-looking statements as a result of uncertainties, risks, and changes in circumstances, including but not limited to risks and uncertainties related to: the impact of fluctuations in global financial markets on CalciMedica’s business and the actions it may take in response thereto; CalciMedica’s ability to execute its plans and strategies; the ability to obtain and maintain regulatory approval for CalciMedica’s product candidates; results from clinical trials may not be indicative of results that may be observed in the future; potential safety and other complications from CalciMedica’s product candidates; economic, business, competitive, and/or regulatory factors affecting the business of CalciMedica generally; CalciMedica’s ability to protect its intellectual property position; expected length of IP protection for CalciMedica’s product candidates; the impact of government laws and regulations; and CalciMedica’s cash runway and need for additional capital. Additional risks and uncertainties that could cause actual outcomes and results to differ materially from those contemplated by the forward-looking statements are included under the caption “Risk Factors” in CalciMedica’s most recently filed periodic report, and subsequent periodic reports filed by CalciMedica, under the Securities Exchange Act of 1934, as amended, from time to time and available at www.sec.gov. These documents can be accessed on CalciMedica’s web page at calcimedica.com. These forward-looking statements are based on information available to, and expectations of, CalciMedica of the date of this presentation. CalciMedica disclaims any obligation to update these forward-looking statements, except as may be required by law.
Pioneering CRAC channel inhibition in Pulmonary Hypertension PLATFORM Leader in CRAC channel inhibition Proven Orai1 / CRAC inhibitor clinical experience Proprietary chemistry and internal pipeline Two current drug candidates: CM5480 (oral) and Auxora (IV) IP out to 2041+ (Auxora) and 2046+ (CM5480) DISEASE BIOLOGY Central to PH pathology Orai1 upregulated in diseased pulmonary vasculature, RV, and LV1 Linked to proliferation, inflammation, vasoconstriction and hypertrophy Relevant to RV failure—key outcomes driver2 DIFFERENTIATION Anti-remodeling in both lung & heart CRAC inhibition activity in both lung and heart tissue Potential direct RV support and anti-remodeling Broad PH potential across disease groups DEVELOPMENT STRATEGY Fast human POC data, followed by optimized oral development Auxora IV Ph1b POC in PAH expected mid-2027 CM5480 oral IND targeted mid-2027; data expected mid-2028 Auxora POC trial designed to de-risk CM5480 in PH and potentially advance Auxora for hospitalized PH Key Anticipated Catalysts: Auxora Ph1b data in PAH (mid-2027) | CM5480 IND clearance (mid-2027) 1. Saint-Martin Willer et al., JCI Insight 2025; Masson et al., Circ Res 2022; Bartoli et al., Circulation 2020; Antigny et al., Circulation HF 2025 2. Vonk Noordegraaf A, et al. Cardiovascular Research 2015 RV = Right Ventricle; LV = Left Ventricle; PH = Pulmonary Hypertension; POC = Proof of Concept
Two well-characterized drug candidates, built on deep CRAC channel expertise CLINICAL · IV Auxora Zegocractin · 4-hour infusion, 3–5 days CLINICAL EVIDENCE Multiple Phase 2 trials: acute pancreatitis, COVID-19 pneumonia, and acute kidney injury Statistically significant reduction in severe respiratory failure observed across studies BIOMARKER VALIDATION Normalized inflammatory cytokines (IL-6, TNF-α, IL-17) Improved markers of endothelial damage and microcoagulation (D-dimers, Ang-1, Ang-2) PRECLINICAL · ORAL CM5480 Selective, potent oral CRAC inhibitor PRECLINICAL EVIDENCE Active across PAH, rheumatoid arthritis, ulcerative colitis, asthma, and chronic pancreatitis PHARMACOLOGY Anti-inflammatory, tissue-protective, and anti-proliferative activity PK, dosing, and toxicology conducted in three species (unpublished) DEVELOPMENT STATUS IND-enabling and formulation studies ongoing Link between the two assets: Potential for Auxora to de-risk CM5480 in Pulmonary Hypertension
PH-focused pipeline designed to generate human POC data by mid-2027 with next-gen compound to follow Program Preclinical Phase 1 Phase 2 Phase 3 Anticipated Milestones Auxora – IV1 Pulmonary Arterial Hypertension IND clearance – 2H 2026 Ph1b POC data – mid 2027 CM5480 – Oral Pulmonary Arterial Hypertension IND clearance – mid-2027 CM5480 – Oral CpcPH-HFpEF IND clearance – mid-2027 Auxora – IV Acute Pancreatitis FDA feedback on potential pivotal program design – Q3 2026 Future development pending funding Pulmonary Hypertension Acute Critical Disease 1: Auxora Ph1b trial not yet initiated; IND clearance anticipated 2H 2026
CRAC channels: A store-operated calcium signaling system STIM1 (ER Ca²⁺ sensor) Endoplasmic reticulum Plasma membrane Ca2+ release channels Orai1 (Ca2+ channel) Ca2+ CRAC channels are “store-operated”: their activity is controlled by the level of Ca²⁺ in the endoplasmic reticulum (ER), the cell’s internal Ca²⁺ store. During normal receptor signaling, ER Ca²⁺ release lowers ER Ca²⁺ levels. STIM1 senses that drop and activates Orai1 at the plasma membrane, allowing extracellular Ca²⁺ to enter the cell. 1 2 3 The incoming Ca²⁺ both helps refill the ER and sustains normal, tightly regulated cellular programs — including activation, secretion, migration/repair, and gene regulation. Adapted from Roos,…Stauderman, J. Cell Bio. 2005; Zhang…Stauderman, Cahalan, Nature, 2005; Zhang…Stauderman, Cahalan, PNAS, 2006. In healthy cells, CRAC signaling is tightly regulated, localized, and self-limited
Disease can overdrive CRAC channel signaling, creating a persistent, pathologic calcium signal Persistent receptor signaling in inflammatory settings Cell stress Phenotypic change Persistent Orai1-mediated Ca²⁺ influx generates a disease-driving calcium signal1 Inflammatory activation Direct tissue injury Barrier / microvascular dysfunction Vascular and Ventricular (RV and LV) remodeling Cells decode this signal through calcineurin/NFAT, NF-κB, mitochondrial stress pathways, and barrier/remodeling machinery DISEASE OVERDRIVES CRAC CHANNEL SIGNALING PERSISTENT CRAC CHANNEL SIGNALING RESULTS 1. Masson et al., Circulation Research 2022 (among others) RV = Right Ventricle; LV = Left Ventricle
Pulmonary Hypertension spans diverse etiologies, but RV failure drives prognosis across groups Group 1 Pulmonary Arterial Hypertension (PAH) Idiopathic • Heritable • CTD-associated • Drug-induced Group 2 PH due to Left Heart Disease HFpEF, including CpcPH-HFpEF • HFrEF • Valvular disease Group 3 PH due to Lung Disease / Hypoxia COPD • ILD • Sleep-disordered breathing Group 4 PH due to Pulmonary Artery Obstruction CTEPH • Chronic thromboembolic disease Group 5 PH with Unclear / Multifactorial Mechanisms Sarcoidosis • Hematologic / metabolic disorders Why it matters: RV function is a major determinant of symptoms, functional decline & survival across PH groups Therapeutic gap: Current therapies primarily target the pulmonary circulation — not the failing RV directly CalciMedica opportunity: CRAC channel inhibition is active in both pulmonary vascular and RV tissue, creating the potential for a differentiated lung–heart profile Shared consequence across PH pathologies: progressive right ventricular failure Elevated pulmonary pressures RV pressure overload RV remodeling & dysfunction RV failure Initial Development Pathways
CRAC channel inhibition as a potential therapy for PAH "These preclinical results show that targeting Orai1 delivered several key benefits: it improved pulmonary vascular remodeling by reducing pulmonary arterial smooth muscle cell and pulmonary endothelial cell dysfunctions; it improved RVD; and combination therapy with CM5480 provided significantly greater benefits…compared to monotherapies.“ "Despite recent improvements in the treatment of PAH, it remains a severe disease for which there is no cure, and patients often progress to RVF. We continue to search for new potential drugs with novel mechanisms that can enhance current treatment strategies. Our translational work has suggested that CRAC channel inhibition could offer such a mechanism" Dr. Marc Humbert, Université Paris-Saclay, INSERM Dr. Fabrice Antigny, Université Paris-Saclay, INSERM Over a decade of research by a world-class team at INSERM supports CRAC channel inhibition in pulmonary hypertension (select publications highlighted in next slide)
CRAC channel inhibition shows activity across pulmonary vasculature, RV, and LV in preclinical PH models 1. Saint-Martin Willer et al., JCI Insight 2025 2. Masson et al., Circ Res 2022 3. Research results from INSERM lab conducted by Antigny and Sabourin; shared with permission. Unpublished data 4. Bartoli et al., Circulation 2020 PVR = Pulmonary Vascular Resistance; RVSP = RV Systolic Pressure; TAPSE = Tricuspid Annular Plane Systolic Excursion; FAC = Fractional Area Change; EF = Ejection Fraction; FS = Fractional Shortening; MOA = Mechanism of Action; RVF = Right Ventricular Failure Model Observations Why it matters MCT rat (CM5480)1 PVR ↓ Cardiac output restored RV hypertrophy ↓ RV fibrosis ↓ RNA-seq: broad reversal of disease-associated genes in lung and RV Widely used and standard PAH model CM 5480 observed to improve lung and cardiac function and showed anti-remodeling activity in both lung and RV Additive benefit when combined with sildenafil or ambrisentan Sugen/Hypoxia rat (tool compounds)2 PVR ↓ Cardiac output restored RVSP ↓ Pulmonary vascular remodeling ↓ RV hypertrophy ↓ RV fibrosis ↓ Su/Hx is considered the most clinically translatable PAH model Reproducibility across a second preclinical PAH model supports the robustness of the observed effect In prior preclinical studies, CM5480 demonstrated activity consistent with the tool compounds evaluated in these models Pulmonary artery banding rat (CM5480)3 RV systolic function ↑ (TAPSE, FAC) RV diastolic function ↑ RV hypertrophy ↓ RV fibrosis ↓ PAB isolated the RV effect from any pulmonary vascular effect Evidence of direct RV benefit extends the potential opportunity from Group 1 to any PH-driven RV failure Potential differentiation vs. TGF-β/activin MOA Transverse aortic constriction mouse (tool compound)4 LV systolic function preserved (EF, FS) End-systolic volume ↓ Fibrosis ↓ Improved LV-arterial coupling Normalized Ca²⁺ handling Established that the cardiac protective effect generalizes from RV to LV under pressure overload Provided mechanistic rationale for Group 2 PH (PH-LHD) In addition, gene expression data from patient tissues, model animal tissues, and knock-out models offer further evidence of CRAC channel involvement in PH disease processes
CRAC channels (Orai1/STIM1) are upregulated in lung vasculature in patients with PAH & PVOD PVOD = Pulmonary Veno-Occlusive Disease; Masson et al., Circulation Research 2022 and Saint-Martin Willer et al., JCI Insight 2025 Lung Tissues from PAH Patients Lung Tissues from PVOD Patients Control PVOD
Additionally, CRAC channels (Orai1/STIM1) are upregulated in both sides of the heart when under pressure overload Note: Glycosylated form of Orai1 refers to functional (membrane-localized) Orai1; STIM1L is a long splice isoform of STIM1 that enables faster, repetitive SOCE activation. Sources: Bartoli et al, Circulation 2020 (TAC mouse, Fig 1B–C) · Antigny et al, Circ Heart Fail 2025 (human PAH RV, Fig 8C) · Sabourin et al, J Mol Cell Cardiol 2018 (monocrotaline rat, Fig 7A) Right-Ventricle Left-Ventricle Transverse aortic constriction (TAC) mouse model forces the LV to pump against high pressure Monocrotaline (MCT) rat model causes pulmonary vascular disease, forcing RV to pump against high pressure (PAH model) Human RV tissue from PAH patients obtained at heart-lung transplant, representing end-stage RV pressure overload in the clinical disease
Prior studies linked Orai1 to remodeling/hypertrophy in both the pulmonary arteries and the heart Masson et al., Circ Res 2022;131:e102–e119; Voelkers et al., J Mol Cell Cardiol 2010;48:1329–1334 PASMC = Pulmonary Artery Smooth Muscle Cell PASMCs: Orai1 inhibition reverses proliferative, migratory, apoptosis-resistant phenotype Cardiomyocytes: Orai1 silencing blocks hypertrophic growth In vivo MCT rats (top); human PAH-PASMCs (bottom) Neonatal rat cardiomyocytes, PE-induced hypertrophy
CM5480 demonstrated anti-remodeling activity in the lung and showed reduction in pulmonary vascular resistance (PVR) in MCT PAH model Note: PVR (Pulmonary Vascular Resistance) = RVSP / CO CM5480 as Monotherapy Reduced PVR CM5480 in Combination with SOC Reduced Pulmonary Vascular Remodeling PVR Reduced PVR Reduced Pulmonary Vascular Remodeling PVR CM5480 Monotherapy observed to reduce PVR and pulmonary vascular remodeling Combination with two SOC drugs showed additive benefit
CM5480 has been shown to improve cardiac output and RV remodeling in MCT PAH model 1. Fulton index and RV/tibia length measure RV hypertrophy; Fulton index = weight ratio of RV to the sum of the LV + septum Publication: Saint-Martin Willer et al., JCI (Journal of Clinical Investigation) Insight 2025 Reduced Right Ventricular (RV) Remodeling Improved Cardiac Output CM5480 as Monotherapy CM5480 in Combination with SOC Reduced Right Ventricular (RV) Remodeling1 Improved Cardiac Output CM5480 Monotherapy observed to improve cardiac output and reduce right ventricular remodeling Combination with two SOC drugs showed additive benefit
CM5480 demonstrated direct RV-protective activity in the PAB model 1. From CalciMedica discussions with INSERM team; MOA = Mechanism of Action Source: F. Antigny and J. Sabourin (INSERM), personal communication; shared with permission. Unpublished data. Purpose of Model Endpoints Assessed CM5480 Demonstrated Effect Enables assessment of RV activity independent of pulmonary vascular effects RV systolic and diastolic function RV hypertrophy and remodeling RV fibrosis Hemodynamic parameters Improved RV function Reduced RV hypertrophy Reduced RV fibrosis Consistent with direct RV-protective activity CM5480 showed direct RV benefit in a model isolating RV protection; inhibitor of TGF-β/activin receptor kinases (sotatercept related-MOA) did not show comparable effects in the same model at the same institution1 The pulmonary artery banding (PAB) rat model created fixed RV pressure overload without primary pulmonary vascular remodeling, enabling assessment of direct RV effects independent of the pulmonary vasculature
Left ventricular function rescue under pressure overload: Rationale for CRAC channel inhibition in Group II PH TAC mouse model surgically induced LV pressure overload and systolic dysfunction mimicking LV pathology in Group II PH Orai1 inhibition preserved LV systolic function and improved left ventricular efficiency EJECTION FRACTION 56.9% → 71.2% +14.3 pts p = 0.001 Systolic pump function restored toward sham END-SYSTOLIC VOLUME 0.089 mL → 0.044 mL −51% p = 0.003 Less residual blood after each contraction LV–ARTERIAL COUPLING 1.36 → 2.86 2.1× efficiency SV / ESV Greater stroke output per unit of end-systolic volume TAC MOUSE MODEL | 3-WEEK JPIII INFUSION | N = 5/ARM Parameter (TAC) Vehicle JPIII P-value Heart rate (bpm) 534 ± 16 543 ± 15 0.68 Ejection fraction (%) 56.9 ± 1.3 71.2 ± 3.8 0.001 LV internal diameter, end-systole (mm) 3.27 ± 0.12 2.82 ± 0.17 0.036 End-systolic volume (mL) 0.089 ± 0.008 0.044 ± 0.011 0.003 End-diastolic volume (mL) 0.21 ± 0.022 0.17 ± 0.02 0.12 Stroke volume (mL) 0.121 ± 0.013 0.126 ± 0.005 0.76 Note: JPIII: small-molecule Orai1 inhibitor used as tool compound for target validation Bartoli F et al, 2020 Circulation
CM5480 reversed PAH-mediated genetic changes in both the lung and right ventricle of the heart Publication: Saint-Martin Willer et al., JCI (Journal of Clinical Investigation) Insight 2025 CM5480 is potentially disease-modifying and potentially restores RV function in PAH Transcriptomic profiling of CM5480 Treatment in the MCT Rat Model of PAH 305 dysregulated genes in the lung were restored by CM5480 in MCT-treated rats (vs. 100 with amplified dysregulation) Pathways restored include metabolism and inflammation/immune response 2,358 dysregulated genes in the RV were restored by CM5480 in MCT-treated rats (vs. only 9 with amplified dysregulation) Restoration of gene expression was most striking in the RV Pathways restored include inflammation and heart contraction
Efficient path to potentially validate CRAC channel inhibition in PH and expand across multiple indications Note: Lighter shading indicates activities not reflected in the current cash runway. 2025 2H Preclinical & IND-enabling CMC, tox, translational models Ph1/1b Healthy volunteers + patient cohort(s) Ph2 PAH Ph2 CpcPH-HFpEF PVOD Registrational 2026 2027 2028 2029 1H 2H 1H 2H 1H 2H 1H IND CM5480 (Oral — next-generation, optimized for chronic dosing) Data PAH Ph1b n~10, FC II–III CpcPH-HFpEF Ph1b n~10, FC II–III Data Data AUXORA Ph1b’s (IV — established asset, >350-pt safety database) Potential follow-on trials in hospitalized PH Anticipated Milestones Add’l data
Auxora Ph1b: PAH data with CRAC channel inhibitor anticipated by mid-2027 1. Measurement frequency dependent on endpoint RHC = Right Heart Catheterization; CMR = Cardiac Magnetic Resonance; TAPSE = Tricuspid Annular Plane Systolic Excursion; mPAP = mean Pulmonary Artery Pressure; PCWP = Pulmonary Capillary Wedge Pressure; CI = Cardiac Index Capital-efficient Ph1b study using an established IV asset with a >350-patient safety database — delivering potential first-in-human CRAC channel inhibitor signals in pulmonary arterial hypertension expected in mid-2027 STRATEGIC OBJECTIVES De-risk CM5480 in PAH First potential human signal for CRAC channel inhibition in PAH — expected to inform and de-risk our oral chronic-dosing program (IND clearance anticipated mid-2027). Establish Auxora as a potential IV therapy in hospitalized PH Potential acute / decompensating indications; high unmet need; registration studies could begin in 2027. POPULATION PAH Functional class II and III ~10 patients Baseline PVR ≥5 Wood units Stable on SOC incl. sotatercept TREATMENT 5-day IV course Single treatment course IV infusion daily for 5 consecutive days Administered in Phase 1 unit ENDPOINTS RV and LV hemodynamics RHC / ECHO / CMR + biomarkers LV & RV function: contractility, strain, TAPSE, RA size Hemodynamics: PVR, mPAP, PCWP, CI EmPHasis-10 questionnaire NT-proBNP, Cystatin-C Assessed at Day 5, weekly, and Day 351 ANTICIPATEDTIMELINE Data mid-2027 Advancing to IND submission YE 2026: Trial enrolling Mid-2027: Data
Anticipated milestones Auxora in PAH Ph1b proof-of-concept data extpected mid-2027 CM5480 in PH Additional preclinical data in PH models expected 2H 2026 IND submission expected mid-2027 Cash Runway Cash expected to fund current operations into 2H 2027 Auxora in AP FDA feedback on pivotal program design expected in 3Q 2026
Appendix: Auxora for Acute Pancreatitis (AP)
AP: common, costly, and without approved treatments 1, Peery AF et al. Gastroenterology. 2022;162(2):621–44; 2. Machicado JD et al. United European Gastroenterol J. 2021;9(2):139–49.; 3. Singh VK et al. Clin Gastroenterol Hepatol. 2009;7(11):1247–51.; 4. Boxhoorn L et al. Lancet. 2020;396(10252):726–34; 5. Metri A et al. Surg Open Sci. 2024;19:109–17.; SIRS = Systemic Inflammatory Response Syndrome Respiratory Failure Multi-Organ failure Pancreatic Necrosis Mortality Extended hospital stay US patients per year ~60K4,5 Progress in disease severity Moderate and severe AP ~300K1 Hospitalized for AP Mild Acute Pancreatitis ~170K2,3 Develop SIRS AP with SIRS Economic burden: >1M hospital days and ~$2.5B in U.S. costs annually Calcium-dependent inflammatory cascade drives disease progression
CARPO Phase 2b clinical trial in AP with SIRS Endpoints Time to solid food tolerance (primary endpoint) Severe organ failure Respiratory failure Length of hospital stay Time to medically indicated discharge Necrosis Primary Objective: Dose Response on Primary and Secondary Endpoints Daily in-patient assessments until discharge or Day 30 In person visit CT scan on Day 30 Monitoring for rehospitalizations and other medical issues Screening Assess for SIRS Baseline CT scan 1:1:1:1 N = 216 High Dose Auxora 2 mg/kg Days 1-3 Medium Dose Auxora 1 mg/kg Days 1-3 Low Dose Auxora 0.5 mg/kg Days 1-3 Matching Placebo SIRS: Systemic Inflammatory Response Syndrome
Auxora prevented new severe respiratory failure Observed 100% reduction in new severe respiratory failure1 Observed 60% reduction in severe organ failure2 1. mITT excluding baseline respiratory failure (n=197) 2. mITT (N=214); severe organ failure includes severe respiratory failure, severe renal failure, and severe cardiovascular failure Each p<0.05
Win-ratio analysis favors Auxora across key clinical outcomes Win-ratio (Finkelstein-Schoenfeld): Patient pairs compared hierarchically across endpoints. Percentages represent proportion of comparisons won. Totals <100% because 10.3% of comparisons were ties. CI = confidence interval Endpoint Placebo (n = 53) Auxora 2.0 mg/kg (n = 52) Favored arm All-cause mortality - - (no events) New onset severe respiratory failure 0.0% 7.5% ü Auxora New onset necrotizing pancreatitis 13.6% 22.3% ü Auxora Time to medically indicated discharge 19.8% 26.5% Auxora Across all hierarchical comparisons 33.4% 56.3% Auxora Win-Ratio = 1.64 (95% CI: 1.03–2.61, p = 0.037) % of patient-pair comparisons won
Advancing towards a potential pivotal program in AP Ongoing constructive discussions with the FDA regarding the design of a pivotal program in AP Leveraging AI-enabled analyses with Telperian to refine patient selection and endpoint strategy, with the goal of an enriched, efficient study design FDA feedback on pivotal program design expected in 3Q 2026
Appendix: Additional Slides
To-date, CRAC channel pathway demonstrated that it does not interfere with and is not modulated by pathways targeted by existing PAH therapies PASMC = pulmonary artery smooth muscle cell Publication: Saint-Martin Willer et al., JCI (Journal of Clinical Investigation) Insight 2025 Drug Class Drug Orai1 Protein Expression PDE5 inhibitor Sildenafil Increased Endothelin inhibitor Ambrisentan No effect Monoclonal antibody inhibitor of activin type II receptors Bimagrumab No effect Tyrosine kinase inhibitor Imatinib No effect mRNA Effect of Orai1 Knockdown Endothelin Receptor Type A No change Endothelin Receptor Type B No change Phosphodiesterase 5 (PDE5) No change BMPR2 No change BMPR1A No change TGFBR2 No change TGBR3 No change TGFBR1 Decreased Effect of Orai1 Knockdown on mRNA Expression of Targeted Pathways in Human PAH-PASMCs Effect of PAH Drugs on Orai1 Protein Expression in Human PAH-PASMCs