BriaCell Therapeutics Corp 10-K for FY2022

BriaCell Therapeutics Corp. (BCTX)

10-K 2022-10-28 For: 2022-07-31

Added on April 12, 2026

About this 10-K

BriaCell Therapeutics Corp filed this 10-K on October 28, 2022, covering the fiscal year ended July 31, 2022 (FY2022).

Headline figures

Fiscal year ended July 31, 2022, as reported in this filing, compared with the same period a year earlier where the filing states it.

Net loss: $26.84M; compared with a net loss of $13.82M a year earlier

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British Columbia		47-1099599
(State or other jurisdiction of incorporation or organization)		(I.R.S. Employer Identification No.)

Suite 300 – 235 15^th Street West Vancouver, BC V7T 2X1		V7T 2X1
(Address of principal executive offices)		(Zip Code)

Title of each class		Name of each exchange on which registered
Common Shares, no par value		The NASDAQ Capital Market
Warrants to purchase common shares, no par value		The NASDAQ Capital Market

Securities registered pursuant to Section 12(g) of the Act: None

		Page
	PART I
Item 1	Business	5
Item 1A	Risk Factors	40
Item 1B	Unresolved Staff Comments	58
Item 2	Properties	58
Item 3	Legal Proceedings	58
Item 4	Mine Safety Disclosures	58

	PART II
Item 5	Market for Registrant’s Common Equity, Related Stockholder Matters and Issuer Purchases of Equity Securities	59
Item 6	[Reserved]	59
Item 7	Management’s Discussion and Analysis of Financial Condition and Results of Operations	59
Item 7A	Quantitative and Qualitative Disclosures About Market Risk	67
Item 8	Financial Statements and Supplementary Data	67
Item 9	Changes In and Disagreements with Accountants on Accounting and Financial Disclosure	67
Item 9A	Controls and Procedures	67
Item 9B	Other Information	67
Item 9C	Disclosure Regarding Foreign Jurisdictions that Prevent Inspections.	67

	PART III
Item 10	Directors, Executive Officers, and Corporate Governance	68
Item 11	Executive Compensation	77
Item 12	Security Ownership of Certain Beneficial Owners and Management and Related Stockholder Matters	79
Item 13	Certain Relationship and Related Transactions, and Director Independence	80
Item 14	Principal Accountant Fees and Services	81

	PART IV
Item 15	Exhibits	82
Item 16	Form 10-K Summary	83

SIGNATURES		84

●	We have a history of losses, may incur future losses and may not achieve profitability;
●	We are an early stage development company;
●	We are developing novel technologies which may not be effective or safe;
●	We have an unproven market for our product candidates;
●	We are heavily reliant on third-parties to carry out a large portion of our business;
●	Pre-clinical studies and initial clinical trials are not necessarily predictive of future results;
●	We must obtain additional capital to continue our operations;
●	We are highly dependent on our key personnel;
●	We may not succeed in completing the development of our products, commercializing our products or generating significant revenues;
●	We may not successfully develop, maintain and protect our proprietary products and technologies;
●	Changes in legislation and regulations may affect our revenue and profitability;
●	If we or our licensees are unable to obtain U.S., Canadian and/or foreign regulatory approval for our product candidates, we will be unable to commercialize our therapeutic candidates;
●	Clinical trials involve a lengthy and expensive process with uncertain outcomes, and results of earlier studies and trials may not be predictive of future trial results;
●	Future issuance of our common shares could dilute the interests of existing shareholders; and
●	We have a significant number of options and warrants outstanding, and while these options and warrants are outstanding, it may be more difficult to raise additional equity capital.

	●	There are 150,000 women with metastatic breast cancer in the U.S.¹⁰
	●	~45% will receive third line therapy¹¹ = 68,000 patients available
	●	68,000 x 50% (matched for 1 HLA allele group)¹² = 34,000 patients available for treatment¹³
	●	40% have grade I/II tumors¹⁴= 13,600 patients available for treatment

Study	Treatment & Design	# of Pts		ORR			PFS/TTP		OS
Perez¹⁵	Paclitaxel Monotherapy		212		21.5	%		4.7 mo		12.8 mo
Seidman¹⁶	Gemcitabine Monotherapy		160		26	%
Zelek¹⁷	Vinorelbine Monotherapy		40		25	%				6 mo
Licchetta¹⁸	Cyclophosphamide and megestrol acetate		29		31	%		7.4 mo		13.4 mo
Harvey¹⁹	Docetaxel Monotherapy 60 mg/m2		122		22.1	%		12.7 wk		10.6 mo
	Docetaxel Monotherapy 75 mg/m2		146		23.3	%		15.0 wk		10.3 mo
	Docetaxel Monotherapy 100 mg/m2		139		36.0	%		16.6 wk		12.3 mo
Rivera²⁰	Docetaxel Monotherapy q3wk		59		35.6	%		5.7 mo		18.3 mo
	Docetaxel Monotherapy qwk		59		20.3	%		5.5 mo		18.6 mo
Gradishar²¹	ABI-007 (Nab paclitaxel)		229		33	%		23.0 wk		65.0 wk
	Paclitaxel Monotherapy		225		19	%		16.9 wk		55.7 wk
	ABI-007 (Nab paclitaxel) 2nd line		132		27	%		20.9 wk		56.4 wk
	Paclitaxel Monotherapy 2nd line		136		13	%		16.1 wk		46.7 wk
Perez²²	Ixabepilone Monotherapy		126		11.5	%		3.1 mo		8.6 mo
Leyland-Jones²³	Trastuzumab with paclitaxel		32		59	%		12.2 mo
von Minckwitz²⁴	Trastuzumab with capecitabine		78		48.1	%		8.2 mo		25.5 mo
	Capecitabine Monotherapy		78		27.0	%		5.6 mo		20.4 mo
Verma²⁵	Trastuzumab emtansine		495		43.6	%		9.6 mo		30.9 mo
	lapatinib plus capecitabine		496		30.8	%		6.4 mo		25.1 mo
Geyer²⁶	Lapatinib plus capecitabine		163		22	%		8.4 mo
	Capecitabine Monotherapy		161		14	%		4.4 mo
Bartsch²⁷	Capecitabine and trastuzumab		40		20	%		8 mo		24 mo
Blackwell²⁸	Lapatinib Monotherapy		148		6.9	%		8.1 wk		39.0 wk
	Lapatinib with trastuzumab		148		10.3	%		12.0 wk		51.6 wk

	●	Bria-IMT™ has been evaluated in a regimen including pre-dose low-dose cyclophosphamide (to reduce immune suppression), intradermal inoculation with 20-50 million irradiated Bria-IMT™ cells between two and three days later, with subsequent intradermal inoculation with interferon-α2 approximately two and four days later. This is known as the Bria-IMT™ regimen. Both were single arm studies, so there were no untreated patients for comparison.

	●	BriaCell has evaluated the Bria-IMT™ regimen in two Phase I/IIa studies of Bria-IMT™ in advanced breast cancer patients.

	●	There were four evaluable patients treated in one study (Study SVMC #01-026) and 23 evaluable patients treated in another study (Study WRI-GEV-007) with this regimen with cycles every two weeks for the first month and then monthly. They were heavily pre-treated with a median of four prior systemic therapy regimens.

	●	The data shows an outstanding safety and tolerability profile for Bria-IMT™ in advanced breast cancer patients.

	●	In the SVMC #01-026 study, treatment was limited to six cycles over five months. Four post-menopausal white women were enrolled aged between 58.7 and 73 years. Three had breast cancer and one had Her2+ ovarian cancer. All had failed at least one prior systemic therapy.

	●	These patients received between four and six cycles of treatment on protocol. One patient had an additional 13 cycles off protocol.

	●	The only adverse events that occurred in more than one patient were itch and rash at the inoculation sites. No deaths were reported during this study. There were four serious adverse events (“SAEs”) in 3 patients with one (transient urticaria, grade 3) judged probably related to treatment. All SAEs were manageable with community practice therapies.

	●	The Bria-IMT™ regimen was able to elicit delayed-type hypersensitivity (“DTH”) responses in all patients. DTH is a measure of cell-mediated immunity. This response involves the interaction of T-cells, monocytes, and macrophages. This reaction is caused when CD4+ Th1 helper T cells recognize foreign antigen in a complex with the Class II HLA molecule on the surface of antigen-presenting cells. These can be macrophages or dendritic cells that secrete monokines such as IL-12 and IL-15, which stimulates the proliferation of additional CD4+ Th1 cells. CD4+ T cells secrete other cytokines including IL-2 and interferon gamma, inducing the further release of other Th1 cytokines, thus mediating the immune response. This results also in the activation of CD8+ T cells which destroy target cells on contact, and activated macrophages which produce hydrolytic enzymes.

	●	The DTH response involves the interaction of T-cells, monocytes, and macrophages. This reaction is caused when CD4+ Th1 helper T cells recognize foreign antigen in a complex with the Class II HLA molecule on the surface of antigen-presenting cells. These can be macrophages or dendritic cells that secrete monokines such as IL-12 and IL-15, which stimulates the proliferation of additional CD4+ Th1 cells. CD4+ T cells secrete other cytokines including IL-2 and interferon gamma, inducing the further release of other Th1 cytokines, thus mediating the immune response. This results also in the activation of CD8+ T cells which destroy target cells on contact and activated macrophages which produce hydrolytic enzymes.

	●	One patient (A002) had a partial response with regression of breast lesions, resolution of lung and soft tissue lesions, and improvement of stability of bone lesions. She completed therapy and 3 months after her last Bria-IMT™ inoculation, imaging studies identified regrowth of tumor notably in the breast, lung, and brain. After consultation with the FDA, the patient was treated off-protocol which also produced tumor regression, including the resolution of brain metastases. The HLA-DRB3 allele of patient A002 matched with that of SV-BR-1-GM and the HLA-DRB1 allele of patient A002 also matched that of SV-BR-1-GM. Her tumor was grade II (moderately differentiated). One other patient on this study (B001) with a grade II tumor had disease limited to bony metastases. She did not have measurable disease but was felt to progress on study.

	●	Median time to tumor progression was 144 days (range 64 – 223 days) for the initial round of treatment. Overall survival was more than 33 months in all patients except B001 (7 months).

	●	The most common adverse events seen were local irritation at the inoculation sites. There was one serious adverse event of gastrointestinal reflux disease possibly related to Bria-IMT™.

	●	Several patients showed evidence of anti-tumor activity of the Bria-IMT™ regimen in spite of their being heavily pre-treated advanced breast cancer patients. Specifically, one patient (designated 01-002) had regression or disappearance of 20 lung metastases, but stable disease in liver metastases (as the liver metastases were the target lesions, she did not qualify as a partial response). She displayed a robust DTH response, had a grade I tumor and matched Bria-IMT™ at 2 HLA loci. One patient (05-002) had a reduction in the size of a breast lesion but progression of a liver lesion and did not meet criteria for a partial response. She also displayed a robust DTH response, had a grade II tumor and matched Bria-IMT™ at 2 HLA loci. One patient (01-005) had a marked reduction in cutaneous involvement but developed restrictive cardiomyopathy (unrelated to study drug) with subsequent mortality. She had a grade III (poorly differentiated) tumor and matched Bria-IMT™ at one HLA locus. She was not on study long enough to be evaluated for her response.

	●	Patients 01-002, 05-002 and 01-005 who showed objective evidence of tumor shrinkage all matched the Bria-IMT™ cell line at least at one HLA locus and all had evidence of DTH responses to Bria-IMT™ and/or the parent cell line (SV-BR-1 – the breast cancer cell line from which Bria-IMT™ was derived). Patients who did not develop a DTH response did not show evidence of tumor shrinkage.

	●	Patients 01-002 and 05-002 had grade I/II tumors. Both of them also had two HLA matches with Bria-IMT™. Two other patients with grade II tumors (patient 03-001 and 06-001) had stable disease on the study and were also considered to have received clinical benefit from the treatment. (Clinical benefit was defined as some evidence of tumor shrinkage (including a mixed response with shrinkage of some tumors but progression of others, as for 05-002) with over 90 days on study; or as stable disease, a partial response or a complete response as per RECIST criteria). Neither 03-001 or 06-001 had HLA matches with Bria-IMT™, suggesting that HLA matching may not be required for clinical benefit in patients with grade I/II tumors. Thus, four of the six patients with grade I/II tumors exhibited clinical benefit. One of the remaining patients showed no evidence of an immune response as evaluated by DTH. Thus, four of the five grade I/II patients able to develop an immune response, as noted by DTH, exhibited clinical benefit.

	●	These preliminary data indicate that the Bria-IMT™ regimen in advanced breast cancer patients is well tolerated, able to elicit an immune response and able to induce reduction in tumor burden.

	●	Another phase I/IIa study (BRI-ROL-001) was initiated evaluating the combination of the Bria-IMT™ regimen with KEYTRUDA® (pembrolizumab). This combination combines the induction of an immune response by Bria-IMT™ (i.e. “putting the foot on the gas” of the immune response) with the ability of KEYTRUDA® to block the PD-1 – PD-L1 immune checkpoint (i.e. to “take the foot off the brakes” of the immune response).

	●	Eleven patients with advanced breast cancer (median of four prior systemic therapy regimens) have been treated with this regimen with cycles every three weeks for a median of three cycles (range 1 – 9 cycles).

	●	Two patients had evidence of tumor regression, both of whom had robust immune responses (as measured by DTH) to Bria-IMT™. Both of them had grade II tumors. One matched Bria-IMT™ at two HLA types (06-005) while the other did not match Bria-IMT™ at any HLA types (06-001, who “rolled over” from the WRI-GEV-007 study where she had stable disease), suggesting that the Bria-IMT™ regimen, when given in combination with a PD-1 inhibitor, may be able to induce tumor regression without an HLA match especially in patients with grade I/II tumors. One additional patient (06-004) in this study had a grade II tumor and was noted to have stable disease. The other seven patients treated had grade III tumors (poorly differentiated). Thus, all three of the patients with grade I/II tumors showed evidence of clinical benefit.

	●	Following the establishment of a collaboration with Incyte Corporation, this study is being altered to evaluate the combination of the Bria-IMT™ regimen with INCMGA00012 (anti-PD-1 antibody similar to KEYTRUDA®) and epacadostat (inhibitor of IDO, which suppresses the immune response). The combination with KEYTRUDA® has been discontinued but may be resumed in other studies.

	●	The data confirms the “HLA Matching Hypothesis” and supports BriaCell’s strategy for the development of Bria-OTS™, BriaCell’s first personalized off-the-shelf immunotherapy for advanced breast cancer.

	●	Bria-OTS™ is under development as an off-the-shelf personalized immunotherapy for advanced breast cancer.

	●	The concept for Bria-OTS™ comes from BriaCell’s work with Bria-IMT™, where BriaCell noted that if a patient “matches” Bria-IMT™ in their HLA type, they were more likely to respond.

	●	HLA molecules are the molecules that start immune responses but are polymorphic – i.e. they are different in different people, although some people will share the same HLA molecules (referred to as HLA alleles or HLA types).

	●	Bria-OTS™ is made from cell lines that are genetically engineered to expresses the immune boosters GM-CSF and interferon-α, as well as specific HLA types (a.k.a. alleles).

	●	Different cell lines are being pre-manufactured to express different HLA types covering >99% of the overall breast cancer patient population.

	●	Using the BriaDX™, a companion diagnostic test performed on the patient’s saliva, the suitable personalized treatment will be selected for each patient for administration.

	●	This approach allows personalized treatment without the need for personalized manufacturing. Additionally, it saves time, and skips expensive and complicated manufacturing procedures associated with other personalized treatments.

	●	Bria-OTS™ cell lines are being engineered and transferred to good manufacturing practice (“GMP”) production in 2022 and commencing clinical evaluation in 2022 (expected authorization by FDA and expected first patient to be dosed in 2022) with safety and efficacy data expected to be released during 2022 and 2023.

	●	Cyclophosphamide 300 mg/m2 intravenously 2-3 days prior to Bria-IMT™ inoculation
	●	Bria-IMT™ 20 million irradiated cells given intradermally split into 4 inoculations (2 in the upper back and 2 in the thighs)
	●	Interferon alpha-2b 10,000 units into each inoculation site 2 and 4 days after the Bria-IMT™ inoculations
	●	Treatment cycles every 2 weeks for four weeks (3 inoculations) then every month.

	●	Used unmodified cell line (parental SV-BR-1 cells) + GM-CSF + cyclophosphamide.

	●	N = 14 late stage, treatment-refractory breast cancer patients.

	●	No significant adverse treatment-associated events, well tolerated.

	●	Median Overall Survival = 12.1 months.

	●	Used Bria-IMT™ (i.e. genetically engineered SV-BR-1 cells – producing GM-CSF) with pre-dose, low dose cyclophosphamide and post-dose local interferon-α to boost the response (the Bria-IMT™ regimen) with cycles every two weeks for four weeks (three inoculations) then monthly up to a total of six cycles.

	●	N = 4 late stage, treatment-refractory (3 breast cancer (2 grade II and 1 grade III), and 1 ovarian cancer) patients.

	●	No significant adverse treatment-associated events, well tolerated.

	●	Median Overall Survival = 35 months.

	●	One robust responder with greater than 90% regression during treatment and a subsequent relapse (upon halting treatment) responded to re-treatment.

	●	This patient matched Bria-IMT™ at a key HLA type (HLA-DR) and had a grade II tumor.

	●	The Bria-IMT™ regimen included pre-dose low-dose cyclophosphamide (to reduce immune suppression), intradermal inoculation with 20-50 million irradiated Bria-IMT™ cells between two and three days later, with subsequent intradermal inoculation with interferon-α2b approximately two and four days later. The majority of adverse events (“AEs”) were limited to expected minor local irritation at the injection sites.

	●	The 23 patients treated with this regimen received cycles every two weeks for the first month and then monthly. They were heavily pre-treated with a median of four prior systemic therapy regimens.

	●	Patients were treated with a median of three cycles of therapy (range 1-8).

	●	The Bria-IMT™ regimen was able to elicit both cellular immune responses (as evidenced by DTH responses in 85% of patients evaluated) and antibody responses (present in 58% of patients evaluated).

	●	There were no serious, unexpected, drug-related AEs.

	●	Disease control was seen in four of twenty patients who match with Bria-IMT™ at one or more HLA locus, including in three of six patients who match Bria-IMT™ at two or more HLA loci, further supporting our “HLA Matching Hypothesis”, and the development of Bria-OTS ™ to single match over 99% and double match approximately 90% of the patient population.

	●	Effectiveness also depends on the ability of the patient to develop an immune response to Bria-IMT™, as measured by DTH to the Bria-IMT™ or to the parental cell line (SV-BR-1). Across both “monotherapy” studies (SVMC #01-026 and WRI-GEV-007), a positive DTH response was noted in 22 patients while five were not responsive.

	●	Results are shown in the tables below, combining the second and third proof of concept studies, both of which used Bria-IMT™ in an identical regimen.

Patients	HLA Match		Disease Control			Disease Control in Immune Responders
N=6		≥2		50	%		75	%
N=20		≥1		25	%		33	%
N=7		0		29	%		29	%
All Patients N=27				26	%		32	%

Patients	Grade I/II		Disease Control
All Patients N=27		8		63	%
Immune Responders (as measured by DTH)
Immune Responders N=22		7		71	%

	●	Bria-IMT™ was dosed in 27 patients (four in 2004-2006, 23 in 2017-2018) as the Bria-IMT™ regimen alone.

	●	Bria-IMT™ has been very well tolerated (over 100 doses given to date).

	●	Tumor regression was seen in patients who were able to mount an immune response and matched Bria-IMT™ at HLA types, confirming our main hypothesis and supporting using HLA typing as a marker to predict who is most likely to respond.

	●	BriaCell continues to monitor their clinical trials, proposing that BriaDx™ would include HLA typing as well as other potential biomarkers (such as tumour grade or the ability to mount a DTH response) to identify the patients most likely to respond to the Bria-IMT™ regimen.

	●	Based on these observations, BriaCell is extending this technology to other types of cancer by developing additional immunotherapy cell lines.

	●	Cell lines currently being genetically engineered include a breast cancer cell line, a prostate cancer cell line, a non-small cell lung cancer cell line and a melanoma cell line.

	●	Initial steps in the genetic engineering have been completed with subsequent steps planned for 2022 and 2023.

	●	IND filings for these immunotherapy cell lines are anticipated starting in 2022.

	●	Thirty percent of all human malignancies display activating RAS mutations, with another 60% showing over-activity of Ras-signaling pathways.³⁸

	●	BriaCell’s novel, proprietary PKCδ inhibitors have shown activity against multiple RAS transformed tumors.³⁹

	●	This target has an attractive safety profile based on in vivo studies and knock out mouse studies.⁴⁰

	●	PKCδ also has potential activity as an immunotherapeutic by blocking TGFβ signaling.⁴¹

	●	PKCδ inhibitors are applicable to specific niche tumor types which provide an accelerated clinical development plan.

	●	Structural aspects of first-generation inhibitor rottlerin and staurosporine ([a] pan-PKC inhibitor) were combined to create second generation inhibitor KAM1.

	●	Third generation inhibitors such as BC-106 have improved potency and selectivity.

	●	Fourth generation inhibitors are under development to optimize their drug-like characteristics.

	●	PKCδ inhibitors lack endothelial cell cytotoxicity, while PKCδ deficient mice develop normally and are fertile. This shows that there is no marked intrinsic toxicity as a result of inhibiting PKCδ.

	●	Candidate selection is anticipated in 2022.

1.	Bria-IMT/OTS™ produces breast cancer antigens (i.e. proteins made by breast cancer cells).

2.	Bria-IMT/OTS™ secretes GM-CSF, which further promotes dendritic cell-based antigen presentation (i.e. boosts the response).

3.	Breast cancer antigens are taken up by dendritic cells and “presented” to CD4+ and CD8+ T cells implicated in tumor destruction.

4.	Bria-IMT/OTS™ directly stimulates cancer fighting CD4+ and CD8+ T cells (i.e. further boosts the response).

5.	Bria-IMT/OTS™ biological activity depends on HLA matching of Bria-IMT/OTS™ and the patient.

	●	A phase I/IIa study was performed evaluating the combination of the Bria-IMT™ regimen with KEYTRUDA® (pembrolizumab). This combination combines the induction of an immune response by Bria-IMT™ (putting the foot on the gas of the immune response) with the ability of KEYTRUDA® to block the PD-1 – PD-L1 immune checkpoint (i.e. taking the foot off the brakes of the immune response).

	●	Eleven patients with advanced breast cancer (with a median of four prior systemic therapy regimens) were treated with this regimen, with cycles every three weeks for a median of three cycles each (range: 1 – 9 cycles).

	●	Two patients had evidence of tumor regression, both of whom had grade II tumors and also had robust immune responses (as measured by DTH) to Bria-IMT™. One matched Bria-IMT™ at two HLA types while the other did not match Bria-IMT™ at any HLA types, suggesting that the Bria-IMT™ regimen, when given in combination with a PD-1 inhibitor, may be able to induce tumor regression without an HLA match, especially in patients with grade I/II tumors. One other patient in this cohort had a grade II tumor and that patient had stable disease. Thus, of the three patients with grade I/II tumors treated with the combination of the Bria-IMT™ regimen with pembrolizumab, all three showed evidence of a clinical benefit, as typically defined in clinical research. BriaCell purchased the KEYTRUDA® for this study without a collaboration with Merck while pursuing other avenues to collaborate with a company that has an anti-PD-1 antibody and/or other immune checkpoint inhibitors to use in combination with the Bria-IMT™ regimen. BriaCell has obtained such an agreement with Incyte Corporation as noted below. Based on this, the combination therapy study (BRI-ROL-001) had been amended to evaluate combination of the Bria-IMT™ regimen with Incyte’s PD-1 inhibitor as noted below. The combination with KEYTRUDA® has been discontinued.

	●	Incyte is providing retifanlimab, an anti-PD-1 monoclonal antibody, for use in combination studies with BriaCell’s lead candidate, Bria-IMT™.

	●	Incyte is a global biopharmaceutical company focused on discovering and developing novel therapeutics in oncology and other serious diseases.

	●	The first twelve patients will receive the Bria-IMT™ regimen in combination with retifanlimab. Once safety of the combination has been established, an expansion cohort of 24 subjects will be evaluated. This expansion cohort will be limited to patients who match Bria-IMT™ at one or more HLA alleles and/or have Grade I/II disease.

	●	Dosing of the novel combinations commenced in the fourth quarter of 2019 and is ongoing.

	●	The Company anticipates safety and efficacy data to be released during 2022 and 2023.

	●	Pending discussions with the U.S. Food and Drug Administration (“FDA”), a registration study focused on, but not limited to, Bria-IMT™, in combination with Incyte’s selected compounds for advanced breast cancer, is planned to commence in late 2022 or early 2023 with the Bria-OTS™ program following by approximately 8-10 quarters.

1.	Compositions comprising SV-BR cells

2.	Therapeutic methods of using said compositions

●	completion of preclinical laboratory tests and animal studies performed in accordance with the FDA’s current Good Laboratory Practices (“GLP”) regulations;

●	submission to the FDA of an Investigational New Drug Application (“IND”), which must become effective before clinical trials may begin and must be updated annually or when significant changes are made;

●	approval by an independent Institutional Review Board (“IRB”) or ethics committee at each clinical site before the trial is begun;

●	performance of adequate and well-controlled human clinical trials to establish the safety, purity and potency of the proposed biologic product candidate for its intended purpose;

●	preparation of and submission to the FDA of a Biologics License Application (“BLA”), after completion of all pivotal clinical trials;

●	satisfactory completion of an FDA Advisory Committee review, if applicable;

●	a determination by the FDA within 60 days of its receipt of a BLA to file the application for review;

●	satisfactory completion of an FDA pre-approval inspection of the manufacturing facility or facilities at which the proposed product is produced to assess compliance with cGMP, and to assure that the facilities, methods and controls are adequate to preserve the biological product’s continued safety, purity and potency, and of selected clinical investigations to assess compliance with current Good Clinical Practices (“GCP”); and

●	FDA review and approval of the BLA to permit commercial marketing of the product for particular indications for use in the United States, which must be updated annually when significant changes are made.

●	Phase 1-The investigational product is initially introduced into healthy human subjects or patients with the target disease or condition. These studies are designed to test the safety, dosage tolerance, absorption, metabolism and distribution of the investigational product in humans, the side effects associated with increasing doses, and, if possible, to gain early evidence on effectiveness.

●	Phase 2-The investigational product is administered to a limited patient population with a specified disease or condition to evaluate the preliminary efficacy, optimal dosages and dosing schedule and to identify possible adverse side effects and safety risks. Multiple Phase 2 clinical trials may be conducted to obtain information prior to beginning larger and more expensive Phase 3 clinical trials. In some cases, FDA will grant preliminary marketing authorization for drugs treating areas of high unmet medical need based on Phase 2 clinical trials. If granted, they will also require confirmatory Phase 3 evaluation post-marketing. BriaCell is evaluating Bria-IMT in patients with breast cancer who have failed at least two prior lines of therapy. In this population there is no approved therapy. Therefore, the development plan for Bria-IMT is an area of high unmet medical need. It is anticipated that BriaCell will not need to complete Phase 3 clinical trials prior to submitting the marketing application for Bria-IMT in patients with advanced breast cancer who have failed at least two prior lines of therapy. In this case, a confirmatory Phase 3 evaluation post-marketing will be required. It is anticipated that this would consist of a randomized, controlled clinical trial of Bria-IMT in combination with immune checkpoint inhibitors compared with best available therapy. However, this design is subject to negotiation with the FDA.

●	Phase 3-The investigational product is administered to an expanded patient population to further evaluate dosage, to provide statistically significant evidence of clinical efficacy and to further test for safety, generally at multiple geographically dispersed clinical trial sites. These clinical trials are intended to establish the overall risk/benefit ratio of the investigational product and to provide an adequate basis for product approval.

●	Phase 4-In some cases, the FDA may require, or companies may voluntarily pursue, additional clinical trials after a product is approved to gain more information about the product. These so-called Phase 4 studies may be made a condition to approval of the BLA.

	●	we may not have adequate financial or other resources to complete the development of our product, including two stages of clinical development that are necessary in order to commercialize our products;

	●	we may not be able to manufacture our products in commercial quantities, at an adequate quality or at an acceptable cost;

	●	we may not be able to maintain our CE mark due to regulatory changes;

	●	we may never receive FDA or Health Canada approval for our intended development plans;

	●	we may not be able to establish adequate sales, marketing and distribution channels;

	●	healthcare professionals and patients may not accept our product candidates;

	●	technological breakthroughs in cancer detection, treatment and prevention may reduce the demand for our product candidates;

	●	changes in the market for cancer treatment, new alliances between existing market participants and the entrance of new market participants may interfere with our market penetration efforts;

	●	third-party payors may not agree to reimburse patients for any or all of the purchase price of our products, which may adversely affect patients’ willingness to purchase our product candidates;

	●	uncertainty as to market demand may result in inefficient pricing of our product candidates;

	●	we may face third-party claims of intellectual property infringement;

	●	we may fail to obtain or maintain regulatory approvals for our products candidates in our target markets or may face adverse regulatory or legal actions relating to our product candidates even if regulatory approval is obtained; and

	●	we are dependent upon the results of ongoing clinical studies relating to our product candidates and the products of our competitors. We may fail in obtaining positive results.

	●	decreased demand for our drugs;

	●	injury to our reputation;

	●	withdrawal of clinical trial participants and inability to continue clinical trials;

	●	initiation of investigations by regulators;

	●	costs to defend the related litigation;

	●	diversion of management’s time and our resources;

	●	substantial monetary awards to trial participants or patients;

	●	product recalls, withdrawals or labeling, marketing or promotional restrictions;

	●	loss of revenue;

	●	exhaustion of any available insurance and our capital resources;

	●	the inability to commercialize any drug candidate; and

	●	a decline in the price of our common shares.

	●	decreased demand for those products;

	●	damage to our reputation;

	●	costs incurred related to product recalls;

	●	limiting our opportunities to enter into future commercial partnerships; and

	●	a decline in the price of our common shares.