8-K

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d) of the

Securities Exchange Act of 1934

Date of report (Date of earliest event reported): November 23, 2015 (November 20, 2015)

GENSPERA, INC.

(Exact name of registrant as specified in Charter)

Delaware	0001421204	20-0438951
(State or other jurisdiction of incorporation or organization)	(Commission File No.)	(IRS Employee Identification No.)

2511 N Loop 1604 W, Suite 204

San Antonio, TX 78258

(Address of Principal Executive Offices)

210-479-8112

(Issuer Telephone number)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2. below):

¨ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

¨ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

¨ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

¨ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Item 8.01 Other Items.

On November 20, 2015, GenSpera, Inc. (the “Company”) announced interim results from the Phase II study investigating the use of mipsagargin (G-202) for the treatment of glioblastoma multiforme. The results were presented in a poster entitled “Phase II study of mipsagargin (G-202), a PSMA-activated prodrug targeting the tumor endothelial cells, in adult patients with recurrent or progressive glioblastoma,” at the Society for Neuro-Oncology Annual Scientific Meeting in San Antonio, Texas. A copy of the press release and the poster presented are attached to this report as Exhibits 99.01 and 99.02, respectively.

Item 9.01 Financial Statements and Exhibits.

Exhibit No.	Description
99.01 99.02	Press Release Dated November 20, 2015. Poster Presented at Conference on November 20, 2015.

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this Report on Form 8-K to be signed on its behalf by the undersigned hereunto duly authorized.

Dated: November 23, 2015

GenSpera, Inc.
By:	/s/ Craig Dionne
	Craig Dionne Chief Executive Officer

INDEX OF EXHIBITS

Exhibit No.	Description
99.01 99.02	Press Release Dated November 20, 2015. Poster Presented at Conference on November 20, 2015.

EX-99.01

Exhibit 99.01

Mipsagargin Demonstrates Clinical Benefit in Subset of Glioblastoma Patients

GenSpera’s Interim Phase II Glioblastoma Data Showcased at
Society for Neuro-Oncology Annual Meeting

SAN ANTONIO, November 20, 2015 — GenSpera Inc. (OTCQB: GNSZ), a biotech company developing a novel prodrug therapeutic for the treatment of cancer, today announced results from the Phase II study investigating the use of mipsagargin (G-202) for the treatment of glioblastoma multiforme. The results will be presented today in a poster entitled, “Phase II study of mipsagargin (G-202), a PSMA-activated prodrug targeting the tumor endothelial cells, in adult patients with recurrent or progressive glioblastoma,” at the Society for Neuro-Oncology (SNO) Annual Scientific Meeting in San Antonio, Texas. The poster is available on the company website.

“We are seeing disease stabilization in a subset of patients and, importantly, clinical benefit appears to be correlated with PSMA expression, which offers enrichment strategies to enroll only potential responders in future clinical trials,” said David Piccioni, M.D, Ph.D., the study’s Principal Investigator. “These results demonstrate mipsagargin’s potential to treat a patient population with few therapy options.”

In addition to Dr. Piccioni, the two-stage, single-arm, open-label study (NCT02067156) is led by neuro-oncologist Santosh Kesari, M.D., Ph.D., and is being conducted at the UC San Diego Moores Cancer Center in La Jolla, Calif. The Phase II results indicate that mipsagargin appears to confer clinical benefit in a subset of patients and is well tolerated by glioblastoma patients. The results are as follows:

• Three of 11 efficacy evaluable patients demonstrated at least stable disease at the first disease assessment (2 stable disease, 1 partial response), one of which has met the primary endpoint of six-month progression-free survival.

• No dose-limiting toxicities have occurred. Preliminary evidence suggests that mipsagargin is well tolerated and may induce disease stabilization or treatment response.

• PSMA (Prostate-Specific Membrane Antigen) staining of tumor tissues shows variability of expression but all three responders have >2+ staining. Biomarker evaluation is ongoing.

“We are very encouraged with the positive results from this interim Phase II trial that demonstrate the tolerability and indications of effectiveness of mipsagargin in advanced brain cancer patients,” said Craig Dionne, Ph.D., chief executive officer at GenSpera. “Mipsagargin is a first-in-class agent with a novel mechanism of action that is unlike any other drug being tested in patients with advanced brain cancer.”

Potential Advantages of Mipsagargin in Glioblastoma Patients

Glioblastoma is the most common and most aggressive malignant primary brain tumor in humans. There are approximately 10,000 new cases of malignant glioblastoma diagnosed each year in the United States and, despite optimal treatment, the median survival for these patients is only 12 to 15 months. Treatment commonly consists of surgery followed by radiation and the drug temozolomide. A few drugs have been approved in patients that have recurrent tumors, but none have been shown to promote long-term tumor stabilization or survival. Glioblastomas are particularly resistant to conventional chemotherapy drugs as most cannot cross the blood-brain barrier. This disadvantage of conventional chemotherapy does not apply to mipsagargin because mipsagargin directly attacks the PSMA-expressing cells of the tumor-associated blood vessels that comprise the blood-brain barrier.

About GenSpera

GenSpera, Inc. is a clinical-stage oncology drug discovery and development company. Its lead drug candidate mipsagargin demonstrated positive data in a Phase II clinical trial in hepatocellular carcinoma (liver cancer) patients and has demonstrated highly encouraging interim data in an ongoing Phase II trial for glioblastoma multiforme (brain cancer). GenSpera's technology platform combines a powerful, plant-derived cytotoxin, thapsigargin, with a patented prodrug delivery system for the targeted release of drug candidates within solid tumors without the side-effect profile of traditional chemotherapeutic agents. Mipsagargin was granted Orphan Drug designation by the U.S. Food and Drug Administration (FDA) in 2013 for evaluation in patients with hepatocellular carcinoma.  

For additional information on GenSpera, visit www.genspera.com and connect on Twitter, LinkedIn, Facebook, YouTube and Google+.

Cautionary Statement Regarding Forward Looking Information

This communication may contain forward-looking statements. Investors are cautioned that statements in this document regarding potential applications of GenSpera's technologies or the future prospects of the company constitute forward-looking statements that involve risks and uncertainties, including, without limitation, risks inherent in the development and commercialization of potential products, uncertainty of clinical trial results or regulatory approvals or clearances, need for future capital, dependence upon collaborators and maintenance of our intellectual property rights and the acceptance of GenSpera’s proposed therapies by the health community. Actual results may differ materially from the results anticipated in these forward-looking statements. Additional information on potential factors that could affect our results and other risks and uncertainties will be detailed from time to time in GenSpera's periodic reports filed with the

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EX-99.02

Exhibit 99.02

• Two stage, single-arm, open label single-institution phase II clinical trial of G-202 in recurrent or progressive glioblastoma • Accrual goal of 34 efficacy-evaluable patients, defined as those that receive two cycles of drug followed by disease assessment • Up to 3 prior recurrences allowed • Primary endpoint: 6 month PFS • Secondary endpoints include safety, efficacy, effects of G-202 on quantitative blood flow metrics, CSF and blood pharmacokinetics, and molecular response correlates • Two regimens were evaluated: 40 mg/m 2 on days 1,2, and 3 of a 28 day cycle, and 40 mg/m 2 on day 1, and 66.8 mg/m 2 on days 2 and 3. Based on tolerability the lower dosing regimen was selected for further evaluation Phase II study of mipsagargin(G-202), a PSMA-activated prodrug targeting the tumor epithelium, in adult patients with recurrent or progressive glioblastoma David Piccioni 1 , Tiffany Juarez 1 , Bradley Brown 1 , Lara Rose 1 , Victoria Allgood 2 , Santosh Kesari 1,3 ; 1 UC San Diego Moores Cancer Center, La Jolla, CA; 2 Genspera, Inc., San Antonio, TX, 3 John Wayne Cancer Institute, Santa Monica, CA. Purpose The purpose of this study is to evaluate the efficacy of G-202, a PSMA-activated prodrug, in recurrent or progressive glioblastoma Background • Glioblastoma is the most common primary malignant brain tumor, and response rates for recurrent disease are poor • PSMA (Prostate-Specific Membrane Antigen) is a transmembrane glycoprotein glutamate carboxypeptidase type II, originally identified in malignant prostate tissue • More recently, PSMA has been identified in the endothelium of many solid tumors, but not in the endothelium of normal tissues, making it an attractive target for antineoplastic therapy • The tumor endothelium of glioblastoma exhibits strong expression of PSMA (Figure 1) • Mipsagargin(G-202) is a thapsigargin prodrug (12ADT) consisting of a cytotoxic analog of thapsigargin coupled to a masking peptide (Figure 2) • 12ADT is a natural product toxin that has been shown to kill a broad spectrum of cancer cell lines by blocking the sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA), leading to apoptosis • PSMA cleaves the thapsigargin analog from its masking peptide at the tumor endothelium, confining the release of the cytotoxinto the tumor vasculature • G-202 is dosed IV on 3 consecutive days every 28 day cycle Results Results Conclusions References Study Design • A two stage design was performed. Two out of the first eleven efficacy-evaluable patients were needed to have at least stable disease to move to stage two. One patient had stable disease and one patient had a partial response (Figure 3, Figure 4). The study was then expanded to a goal of 34 efficacy-evaluable patients. A third patient had stable disease at 2 months. • PSMA staining of the 3 responders has demonstrated > 2+ positivity by IHC • To date, 19 patients have been enrolled and dosed with at least one cycle and are safety-evaluable. Four patients were not efficacy-evaluable. Four additional patients have been recently started on study and have not reached the first disease assessment at 8 weeks. Results Figure 3. Patient 7. Imaging response at 8 months. Partial response. Pre-treatment images on the left. 8 month MRI on the right. Decrease in both contrast enhancement (top) and edema (bottom). Patient continues on trial. Table 1: Adverse Effects = Grade 2,that are possibly, probably or definitely related to the study drug. 19 evaluable patients. • Three of eleven patients demonstrated at least stable disease at the first disease assessment (2 SD, 1 PR), one of which has met the primary endpoint of 6 month PFS • No dose-limiting toxicities have occurred. Preliminary evidence suggests that G-202 is well tolerated and my induce disease stabilization or treatment response • PSMA staining of tumor tissue shows variability of expression but all 3 responders have >2+ staining. Biomarker evaluation is ongoing • The study is currently open and actively enrolling 1. Nomura N, PastorinoS, Jiang P, Lambert G, Crawford JR, GymnopoulosM, Piccioni D, Juarez T, Pingle SC, Makale M, Kesari S. Prostate specific membrane antigen (PSMA) expression in primary gliomas and breast cancer brain metastases. Cancer Cell Int. 2014;14(1):26 2. Andersen TB, Lopez CQ, ManczakT, Martinez K, SimonsenHT. Thapsigargin—from ThapsiaL. to mipsagargin. Molecules. 2015; 20 (4):6113-27. 3. Wernicke AG, Edgar MA, LaviE. Prostate-specific membrane antigen as a potential novel vascular target for treatment of glioblastoma multiforme. Arch PatholLab Med. 2011; 135; 1486-1489. Normal Brain Glioblastoma Figure 1. PSMA-positive vasculature in glioblastoma (Right) but not in the vasculature of normal brain (Left) Figure 2. Structure of G-202. The thapsigargin-derived prodrug (12ADT) is cleaved from the masking peptide by the PSMA enzyme in the tumor endothelium (arrows) Thapsigargin-derived component masking peptide component Grade Adverse Effect 2 3 4 Nausea/Vomiting 1 1 1 Infusion Reaction 1 Fatigue 2 Reflux 1 Rash 2 Hyperglycemia 1 Increased ALT 1 1 Increased Creatinine 1 Diarrhea 1 Post- Contrast FLAIR Post- Contrast Figure 4. Patient 12. Imaging response at 2 months. Stable disease. Pre-treatment images on the left. 2 month MRI on the right. Patient had progression on imaging at 4 months. • The most common grade I AE attributable to the study drug was a transient increase in creatinine in 8 of 19 patients. The remaining grade 2 or greater AEs attributed to the study drug are listed in Table 1.