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CalciMedica’s Common Stock to Begin Trading on a Post-Split Adjusted Basis on August 31, 2026 LA JOLLA, Calif., Aug. 27, 2026 (GLOBE NEWSWIRE) -- 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 it will effect a reverse stock split of its issued and outstanding common stock, at a ratio of 1-for-5, effective at 5:00 p.m. ET on August 28, 2026. CalciMedica’s common stock will begin trading on the Nasdaq Capital Market on a split-adjusted basis commencing upon market open on August 31, 2026 under CalciMedica’s existing trading symbol “CALC” with a new CUSIP number, 38942Q301. The reverse stock split was approved by CalciMedica’s stockholders at CalciMedica’s Annual Meeting of Stockholders held on August 19, 2026, with the final ratio subsequently determined by CalciMedica’s Board of Directors. The reverse stock split is intended to bring CalciMedica into compliance with the minimum bid price requirement for continued listing on the Nasdaq Capital Market. At the effective time of the reverse stock split, every 5 shares of CalciMedica’s issued and outstanding common stock will be automatically combined and converted into one issued and outstanding share of common stock, and the authorized shares of CalciMedica’s common stock will be reduced from 500 million to 100 million shares, without any change in par value per share. The reverse stock split will reduce the number of issued and outstanding shares of common stock from approximately 34.5 million shares to approximately 6.9 million shares. The reverse stock split reduces the number of shares of common stock issuable upon the exercise or vesting of CalciMedica’s outstanding stock options, restricted stock units and warrants in proportion to the ratio of the reverse stock split and causes a proportionate increase in the exercise prices of such stock options and warrants, in accordance with their respective terms and as described in CalciMedica’s proxy statement for its Annual Meeting of Stockholders as filed with the Securities and Exchange Commission on July 23, 2026 (the “Proxy Statement”). No fractional shares of common stock will be issued as a result of the reverse stock split. Stockholders of record who would otherwise be entitled to receive a fractional share will receive a cash payment in lieu thereof. The reverse stock split impacts all holders of the Company’s common stock proportionally and will not impact any stockholder’s percentage ownership of common stock (except to the extent the reverse stock split results in any stockholder owing only a fractional share). The Company has chosen its transfer agent, Equiniti Trust Company, LLC (the “Transfer Agent”), to act as exchange agent for the reverse stock split. Stockholders owning shares via a bank, broker or other nominee will have their positions automatically adjusted to reflect the reverse stock split and will not be required to take further action in connection with the reverse stock split, subject to brokers’ particular processes. Additional information regarding the reverse stock split can be found in the Proxy Statement. About CalciMedica CalciMedica is a clinical-stage biopharmaceutical company developing novel calcium release-activated calcium (CRAC) channel inhibition therapies for serious inflammatory, immunologic, and cardiopulmonary diseases. The Company’s pipeline includes Auxora™, its intravenous CRAC channel inhibitor, and CM5480, its oral CRAC channel inhibitor candidate. Auxora has been evaluated in more than 350 patients and is being developed for pulmonary arterial hypertension and acute pancreatitis, including a planned Phase 1b proof-of-concept trial in PAH and a planned Phase 2b trial in acute pancreatitis. CM5480 is being developed for pulmonary hypertension, with an IND submission anticipated in mid-2027. For more information, please visit Forward-Looking Statements This communication contains forward-looking statements which include, but are not limited to, statements regarding the anticipated effects of the reverse stock split on the number of outstanding shares of CalciMedica’s common stock, the anticipated commencement of trading of CalciMedica’s common stock on a split-adjusted basis, the intended purpose and expected benefits of the reverse stock split, including CalciMedica’s ability to regain compliance with the minimum bid price requirement for continued listing on the Nasdaq Capital Market, the treatment of fractional shares and the proportionate adjustment of outstanding equity awards. 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; expected benefits of the reverse stock split may not be realized; there can be no assurance that the reverse stock split will result in CalciMedica regaining or maintaining compliance with Nasdaq listing requirements; the reverse stock split may not result in an increase in the per share price of CalciMedica’s common stock or such increase may not be sustained; the reverse stock split may decrease the liquidity of CalciMedica’s common stock economic, business, competitive, and/or regulatory factors affecting the business of CalciMedica generally; 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 June 30, 2026, as filed with the SEC on August 11, 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 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. Investor Relations Contact Joyce Allaire LifeSci Advisors, LLC jallaire@lifesciadvisors.com

酒精滥用是全球范围内导致健康损害、疾病和死亡的主要因素之一，其不仅对肝脏造成严重影响，对胰腺的损害同样不容忽视。胰腺作为负责内外分泌功能的关键器官，对酒精及其代谢产物极为敏感。流行病学调查已明确显示，酒精摄入与急性胰腺炎、慢性胰腺炎、胰腺癌以及糖尿病等多种胰腺疾病存在密切关联。全球饮酒率的持续上升，尤其是在中等收入国家的显著增长，预示着未来酒精相关的胰腺疾病负担将愈发沉重。 尽管部分研究曾提出适度饮酒可能具有保护作用的J型曲线假说，但近年来的大规模遗传学与流行病学研究，如全球疾病负担研究，已明确指出最安全的饮酒量为零，任何剂量的酒精摄入均对健康构成风险。酒精已被确认为胰腺炎、胰腺癌及糖尿病的重要可调控危险因素，其致病效应通常呈现剂量依赖性，并与吸烟、遗传易感性、高脂血症及饮食等协同因素相互作用，构成复杂的多因素致病网络。 酒精对胰腺的损伤机制涉及复杂的代谢途径与多细胞靶点。胰腺组织可通过氧化途径与非氧化途径代谢酒精。在氧化途径中，酒精经乙醇脱氢酶转化为乙醛，再经乙醛脱氢酶转化为乙酸，此过程伴随活性氧的大量产生及还原型烟酰胺腺嘌呤二核苷酸与氧化型烟酰胺腺嘌呤二核苷酸比值的改变，导致谷胱甘肽耗竭并诱发内质网应激。细胞色素P450 2E1旁路的激活则进一步加剧了氧化应激。在非氧化途径中，酒精与脂肪酸结合生成脂肪酸乙酯，后者在胰腺内的合成活性远高于肝脏，是导致胰腺特异性损伤的关键毒性产物。这些代谢产物共同作用于胰腺内的多种细胞类型。 在腺泡细胞中，它们通过干扰细胞内钙离子稳态，引发钙离子超载、线粒体功能障碍及三磷酸腺苷耗竭，进而导致胰蛋白酶原提前激活、自噬流受阻和细胞坏死。同时，内质网中未折叠蛋白反应的持续激活虽然具有适应性保护意义，但长期暴露仍可导致细胞凋亡。胰腺星状细胞在酒精刺激下被激活，转化为肌成纤维细胞表型，大量合成α-平滑肌肌动蛋白及细胞外基质成分，并通过自分泌与旁分泌信号环路维持活化状态，最终驱动胰腺纤维化。酒精还可损害胰腺导管上皮的屏障功能与碳酸氢盐分泌，导致胰液粘稠度增加及导管堵塞，同时诱导导管细胞恶性转化。对于胰岛β细胞，酒精通过诱导氧化应激、线粒体功能障碍及内质网应激，导致胰岛素分泌功能受损及细胞凋亡，从而促进糖尿病的发生。 酒精相关胰腺疾病的临床表现与预后具有显著异质性。在急性胰腺炎中，酒精是仅次于胆石症的第二大病因，约占全部病例的17%至25%，并且与更高的多器官功能衰竭风险及死亡率相关。长期大量饮酒是慢性胰腺炎最常见的单一危险因素，通常需要每日摄入超过80克酒精并持续6至12年方可显著增加患病风险。酒精性急性胰腺炎具有更高的复发率和向慢性胰腺炎转化的倾向，而慢性胰腺炎本身又是胰腺癌的重要癌前病变。流行病学数据显示，重度饮酒者罹患胰腺癌的风险较非饮酒者增加约20%。 此外，酒精性胰腺炎患者发生胰源性糖尿病的风险显著高于非酒精性病因患者，且此类糖尿病现已超越1型糖尿病，成为成年人中第二常见的糖尿病类型。遗传多态性在疾病易感性中扮演关键角色，胰蛋白酶原PRSS1、SPINK1及CFTR等基因变异可显著增加酒精对胰腺的损伤效应，解释为何仅约5%的重度饮酒者最终发展为胰腺炎。 针对酒精性胰腺损伤的治疗策略，永久性戒酒仍是所有干预措施中最核心且最有效的基石。大量临床观察表明，戒酒能显著降低急性胰腺炎复发率、延缓向慢性胰腺炎及胰腺癌的进展，并改善患者远期生存。然而，鉴于长期戒酒的临床挑战，针对病理机制的药物研发成为重要补充方向。当前研究方向聚焦于抗氧化剂以中和活性氧，抗炎性细胞因子单克隆抗体如英夫利西单抗与托珠单抗以阻断关键炎症通路，以及钙离子通道抑制剂如CM4620以阻止毒性钙超载。此外，靶向线粒体通透性转换孔的抑制剂如NIM811也在临床前研究中展现出保护线粒体功能与维持能量代谢的潜力。针对肠道菌群失调的干预策略，如益生菌及粪菌移植，亦为新兴探索领域。尽管诸多靶向药物尚处临床试验阶段，但基础研究的持续突破正为开发特异性、有效且安全的治疗方案提供理论依据与潜在靶点。