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Tenax Therapeutics, Inc. (NASDAQ:TENX) Files An 8-K Other Events

Tenax Therapeutics, Inc. (NASDAQ:TENX) Files An 8-K Other Events
Item 8.01

Other Items.
On June 2, 2020, Tenax Therapeutics, Inc. (the “Company”) issued a press release announcing that on May 29, 2020 the Company received top line data results on its Phase 2 clinical study of levosimendan for the treatment of patients with pulmonary hypertension and heart failure with preserved ejection fraction (PH-HFpEF).
The Company also held a webcast call on June 2, 2020 to review the results. A copy of the press release is attached hereto as Exhibit 99.1 and the presentation materials for the webcast call is attached hereto as Exhibit 99.2, both of which are incorporated herein by reference.
Item 9.01
Financial Statements and Exhibits.
(d)
Exhibits
TENAX THERAPEUTICS, INC. Exhibit
EX-99.1 2 tenx_ex991.htm PRESS RELEASE tenx_ex991   Exhibit 99.1     Tenax Therapeutics Reports Positive Results from Phase 2 Trial of Levosimendan in Patients with Pulmonary Hypertension and Heart Failure with Preserved Ejection Fraction (PH-HFpEF)   – Demonstrated a significant reduction in right atrial and pulmonary capillary wedge pressures – Demonstrated a significant improvement with 6-minute walk distance – No significant safety issues.  – Management to host conference call and webcast today at 8:30 a.m. EDT   Morrisville,…
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About Tenax Therapeutics, Inc. (NASDAQ:TENX)

Tenax Therapeutics, Inc. is a specialty pharmaceutical company. The Company is focused on identifying, developing and commercializing products for the critical care market. The Company’s main product is levosimendan. Levosimendan is a calcium sensitizer developed for intravenous use in hospitalized patients with acutely decompensated heart failure. Levosimendan represents therapeutic modalities for the treatment of Low Cardiac Output Syndrome (LCOS), septic shock and other critical care conditions. The therapeutic effects of levosimendan are mediated through increased cardiac contractility by calcium sensitization of troponin C, resulting in a positive inotropic effect, which is not associated with substantial increases in oxygen demand; opening of potassium channels in the vasculature smooth muscle, resulting in a vasodilatory effect on all vascular beds, and opening of mitochondrial potassium channels in cardiomyocytes, resulting in a cardioprotective effect.

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